Podcasts about animal models

Relevant links:Jim Haslam on X: https://x.com/jhas5Jim's Substack: https://jimhaslam.substack.com/Jim's book, "COVID-19: Mystery Solved," on Amazon: https://www.amazon.com/COVID-19-Mystery-Solved-leaked-Chinese-ebook/dp/B0DPVT9LWV?ref_=ast_author_cp_dpChapters:(00:00) - A quick note on my interview with Jim Haslam (03:40) - Introducing Jim Haslam, author of "COVID-19: Mystery Solved" (04:51) - The DARPA DEFUSE Grant Proposal (08:52) - Ralph Baric and Genetic Engineering of Coronaviruses (20:10) - Danielle Anderson and the Wuhan BSL-4 Lab (24:38) - The Role of EcoHealth Alliance and Peter Daszak (29:28) - The Furin Cleavage Site Controversy (36:43) - NIAID Funding and the Wuhan Connection (40:53) - Capabilities and Limitations of the Wuhan Institute of Virology, Baric's Lab (44:41) - The DEFUSE Grant and Wuhan Institute of Virology (48:22) - RaTG13 Genome and Its Implications (50:34) - Kristian Anderson's Alarming Discovery (01:00:42) - Feb. 1 Teleconference with Fauci & Baric; Feb. 3 NAS Meeting (01:19:41) - Unintentional vs. Intentional Engineering (01:21:28) - Tracing the Virus to Wuhan, Patient Zero, and the Role of Danielle Anderson (01:29:38) - Rocky Mountain Lab and Virus Processing (01:36:32) - Animal Models, Engineering Aerosol Transmission (01:42:23) - The Smoking Gun Email

Happy New Year! For many of us, a new year brings a renewed sense of motivation when it comes to health. Earlier this year, Russ sat down to speak with Jonathan Long, a Stanford biochemist who studies the chemicals produced during exercise. The conversation was one of our most popular during 2024 and today we're re-sharing it. As many of us look to create healthy habits in 2025, we hope you'll tune in to hear the exciting research Professor Long is doing to better understand the deep chemical connections between diet, exercise, and human health. Have a question for Russ? Send it our way in writing or via voice memo, and it might be featured on an upcoming episode. Please introduce yourself, let us know where you're listening from, and share your quest. You can send questions to thefutureofeverything@stanford.edu.Episode Reference Links:Stanford Profile: Jonathan Z. LongJohnathan's Lab: LongLab@StanfordConnect With Us:Episode Transcripts >>> The Future of Everything WebsiteConnect with Russ >>> Threads / Bluesky / MastodonConnect with School of Engineering >>> Twitter/X / Instagram / LinkedIn / FacebookChapters:(00:00:00) IntroductionHost Russ Altman introduces guest Johnathan Long, a professor of pathology at Stanford University.(00:01:55) Effective Weight Loss DrugsThe history and development of GLP-1 receptor agonists.(00:03:27) Understanding Metabolism and ExerciseThe role of metabolic chemicals released during physical activity.(00:05:02) Animal Models in Exercise Studies The use of animal models in exercise studies and the discovery of Lac-Phe.(00:06:40) Psychological Preparation for Exercise The psychology of exercise preparation and the involvement of endocannabinoids.(00:08:53) Lac-Phe's Role and Mechanism Lac-Phe's role in suppressing appetite and its production in the gut.(00:11:46) Differences in Exercise Response Exercise response between trained athletes and untrained individuals.(00:12:50) Diabetes and Metabolic Diseases The relationship between diabetes, exercise, and metabolic diseases.(00:14:54) Lac-Phe as a Potential Therapeutic Lac-Phe's potential and parallels to the early stages of GLP-1 drug development.(00:16:13) Importance of How Weight is Lost The importance of losing fat while preserving lean muscle mass.(00:19:04) Exercise as Medicine The need to define physical activity at the same resolution as modern medicines.(00:22:03) Metformin and Exercise Pathways The unexpected connection between metformin and the Lac-Phe pathway.(00:23:53) Prospects of an Exercise Pill The future of an exercise pill, and challenges associated with its development.(00:26:57) Conclusion  Connect With Us:Episode Transcripts >>> The Future of Everything WebsiteConnect with Russ >>> Threads / Bluesky / MastodonConnect with School of Engineering >>>Twitter/X / Instagram / LinkedIn / Facebook

Erin Sharoni joins Ethics Talk to discuss her article: “Which Concepts Are Key to Transitioning From Nonhuman Animal Models to Engineered Microphysiological Systems in Biomedical Research?”  Recorded April 30, 2024.  Read the full article for free at JournalOfEthics.org

Jonathan Long is a biochemist who studies the chemicals produced during exercise. In Long's world, “you always start with molecules,” which offer “clean handles” to understanding complex processes. His lab has identified a chemical produced in the digestive tract during exercise that can make a person stop eating. Long now studies this “gut-brain axis” for ways to treat obesity, diabetes, and, perhaps, even age-related conditions like dementia, as he tells host Russ Altman on this episode of Stanford Engineering's The Future of Everything podcast.Episode Reference Links:Stanford Profile: Jonathan Z. LongJonathan's Lab: LongLab@StanfordStudy on Endocannabinoids and Exercise Motivation: The Endocannabinoid System and Physical ExerciseConnect With Us:Episode Transcripts >>> The Future of Everything WebsiteConnect with Russ >>> Threads or Twitter/XConnect with School of Engineering >>> Twitter/XChapters:(00:00:00) IntroductionHost Russ Altman introduces guest Jonathan Long, a professor of pathology at Stanford University(00:02:30) Effective Weight Loss DrugsThe increase of effective weight loss drugs, and the history and development of these GLP-1 receptor agonists.(00:04:03) Understanding Metabolism and ExerciseOutline of metabolic chemicals released during physical activity and their potential to combat obesity and diabetes.(00:05:38) Animal Models in Exercise StudiesThe use of animal models in exercise studies and the discovery of Lac-Phe.(00:07:15) Psychological Preparation for ExerciseThe psychological aspects of exercise and the involvement of endocannabinoids in exercise motivation.(00:09:28) Lac-Phe's Role and MechanismThe role of Lac-Phe and its production in the gut.(00:12:21) Differences in Exercise ResponseDifferences in exercise response between trained athletes and untrained individuals.(00:13:25) Diabetes and Metabolic DiseasesThe relationship between diabetes, exercise, and metabolic diseases.(00:15:29) Lac-Phe as a Potential TherapeuticThe potential of Lac-Phe as a weight loss drug, and parallels to GLP-1 drug development.(00:16:48) Importance of How Weight is LostWhether the method of weight-loss matters, and the importance of preserving lean muscle mass.(00:19:40) Exercise as MedicineThe concept of exercise as medicine, and defining physical activity at the same resolution as modern medicines.(00:22:39) Metformin and Exercise PathwaysThe unexpected connection between metformin and the Lac-Phe pathway.(00:24:08) Prospects of an Exercise PillThe future of an exercise pill, and the scientific challenges associated with its development.(00:27:33) Conclusion Connect With Us:Episode Transcripts >>> The Future of Everything WebsiteConnect with Russ >>> Threads or Twitter/XConnect with School of Engineering >>> Twitter/X

Moderator: Daniele Martinelli (Pavia, Italy)Guest: Raquel Gil-Gouveia (Oeiras, Portugal)Guest: Antoinette Maassen van den Brink (Rotterdam, The Netherlands)Join us in this episode as Daniele Martinelli engages in a dialogue with esteemed experts, Prof. Antoinette Maassen van den Brink and Dr. Raquel Gil-Gouveia.They delve into animal models—our window into the brain's hidden mechanisms. These models reveal neurotransmitter dynamics and potential triggers, paving the way for novel therapies. Additionally, they explore gender-specific nuances, shaping the understanding and personalized management strategies. By bridging theory to practice, they emphasize collaboration—a path toward better patient outcomes, alleviating the burden of this debilitating condition.

In this ToxChats© podcast, we spoke with Dr. René Meisner, Head of Safety Assessment at Denali Therapeutics, on using both transgenic and disease mouse models in a drug development program. Topics include considerations for program design, regulatory interactions, and the role of these mice moving forward. s for program design, regulatory interactions, and the role of these mice moving forward. 

Stepping off the well-trodden path, Dr. Trisha Van Dusseldorp left the certainty of tenure for the undiscovered potential of industry—and what a journey it's been. Today, she takes us behind the scenes at Bonafide Health, where she's pioneering advancements in women's health, and candidly shares the calculus of her career leap. From the tug-of-war between the allure of academia and the pulse of corporate life to balancing scientific integrity with commercial pressures, Trisha gives the low-down on the pros and cons of working in the industry.00:00:05 Industry Versus Academia00:08:19 Challenges of HR at Bonafide and Pfizer00:15:09 R&D and Clinical Trials Promoting Products00:19:33 Animal Models, Menopause, and Weight Loss00:24:56 Women's Health and Menopause Challenges00:39:13 Brain Fog and Mushrooms in Industry00:45:49 ISSN Conference

Introduction: Guest: Dr. Monica Embers, Director of Vector-Borne Disease Research and Associate Professor at Tulane University with over 20 years of experience. Topic: Lyme Disease - Testing, Treatment, and Beyond. 1. Diving Deep into the World of Lyme Disease Exploring the sophistication of Lyme disease bacteria. Delving into challenges: unique size, shape, and genetic makeup. Differentiating Lyme bacteria from others and comprehending their behavior. 2. Animal Models in Lyme Research The shift towards studying animal models. Addressing the ethical considerations in animal research. Unpacking the variances: How Lyme bacteria impacts rodents vs. humans. 3. Importance of Research for Clinicians Dr. Embers' vision: Equipping clinicians with vital knowledge and tools. Stressing the need for consistency and validity in research. 4. Challenges in Lyme Disease Diagnosis The hurdles in Lyme diagnosis due to the bacteria's elusive nature. The quest for a direct and reliable diagnostic test. Assessing the drawbacks of present diagnostic measures. 5. Treatment Insights Approaching Lyme treatment with a multi-therapeutic strategy. The debate around prolonged antibiotic therapy. Drawing parallels: Lyme disease treatment vs. tuberculosis. 6. Bacteria Behavior and Characteristics Decoding Lyme disease's stationary phase and its defense mechanisms. Discussing the role of biofilms and their link to Bartonella. Exploring whether or not Lyme disease actually forms biofilms. 7. Bartonella and Cancer Unraveling the potential of Bartonella in inducing cellular changes leading to cancer. The journey of ongoing research to decode Bartonella's extensive effects. 8. Chronic Lyme is Real Dr. Embers' groundbreaking work proving that Chronic Lyme disease is a reality and that Lyme bacteria can persist. Dozens of published research papers with irrefutable evidence of chronic Lyme disease. Stay tuned for an enlightening conversation with Dr. Monica Embers as we explore the intricate world of Lyme Disease.

This month's episode focuses on the history of the use of animals in medical science. We start out with an overview of currently available study models, and a short discussion of why animal models remain irreplaceable at this point in time. Mia goes on into the history of animal use in research, with a special focus on the development of ethical considerations. Trigger warning here! There is some talk about animal torture. To round off the episode, we discuss some very exciting, rapidly developing technologies, specifically organoids (

Episode Description: Dive into a riveting exploration of the intricate dance between science, art, and the animal microbiome. Aaron Schacht delves deep into the transformative power of the microbiome in shaping animal health, the innovative strides in drug development, and the mesmerizing blend of genetics and artistry. From the challenges in livestock production to the silent symphony of cells at a genetic rave, join us on a journey that promises to redefine your understanding of biology and creativity. Grow Everything brings to life the bioeconomy when hosts Karl Schmieder and Erum Azeez Khan share stories from the field and interview leaders and influencers in the space.  Life is a powerful force and it can be engineered. What are we creating? Learn more at www.messaginglab.com/groweverything Topics Covered: 00:00:00 - Delving into a World of Art and Biology: Biotech Beginnings 00:05:47 - Merging Education and Creativity: Enhancing Learning through Art 00:07:03 - Efficiency in Biotechnology: Maximizing Outcomes and Value 00:11:08 - Digital Advancements: Meta's Exploration of Cellular Models 00:14:49 - Big Moves in Biomed: Ginkgo-Pfizer and Merck-Daiichi Collaborations 00:18:24 - Unveiling Animal Health: A Rich Resource in Biomedical Research 00:20:02 - A Warm Welcome to the World of Animal Biomedicine 00:25:21 - Pioneering Drug Safety: The Role of Animal Models 00:30:41 - Sustainable Antibiotic Practices in Animal Farming 00:35:41 - Navigating Challenges: Bacterial Solutions and Microbiomes 00:39:55 - Bridging Academia and Industry: Productive Biotech Innovations 00:42:57 - Advancements in Livestock Health: Probiotics and Enzymes 00:45:44 - Introducing New Biological Therapeutics: Navigating USDA Regulations 00:49:23 - Crafting a Progressive Ecosystem: Investing in Animal Health 00:55:43 - Visioning the Future: Merging Animal Health with Financial Sustainability 00:59:21 - The Digital Leap: AI and Microbiome Engineering in Biomedicine 01:03:16 - Flavor Profiles: Unpacking the Animal Microbiome's Influence 01:07:18 - Collaboration in Biotech: Engaging in Thoughtful Panel Discussions Episode Links: LinkedIn Music Genome Project BiomEdit (company site) Depeche Mode (band site) Ed Ruscha (artist site) Chan Zuckerberg Initiative (organization site) Headway (company site) Gingko & Pfizer deal (story site) Merck & Daiichi Sankyo (story site) Gingko & Persephone collaboration (story site) BioCortex - understanding drug-microbiome interactions (company site) Culitvarium - domesticating non-model organisms (company site) Have a question or comment? Message us here: Text or Call (804) 505-5553 Instagram / TikTok / Twitter / LinkedIn / Youtube / GrowEverything website Email: groweverything@messaginglab.com Support here: Patreon Music by: Nihilore Production by: Amplafy Media --- Send in a voice message: https://podcasters.spotify.com/pod/show/messaginglab/message

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.06.23.546104v1?rss=1 Authors: Trinh, D., Israwi, A., Brah, H., Arriola-Villafue, J., Volpicelli-Daley, L., Nash,, Nash, J. E. Abstract: Degeneration of the dopaminergic nigro-striatal pathway and presence of Lewy bodies are pathological hallmarks of Parkinsons disease (PD). Postmortem studies in human tissue have also demonstrated that a decline in mitochondrial number and function is also central to PD pathology. Sirtuin 3 (SIRT3) is a mitochondrial protein deacetylase which has been linked with longevity and cytoprotective effects. SIRT3 serves as a metabolic sensor and regulates mitochondrial homeostasis and oxidative stress, which likely stabilises telomere integrity, delaying senescence. Previously, we have shown that over-expression of SIRT3 rescues motor function and prevents degeneration of dopaminergic neurons in a virally over-expressing mutant (A53T)-alpha-synuclein model of PD. In the present study, we show that in the substantia nigra pars compacta (SNc) of human subjects, SIRT3 levels are negatively correlated with age (p less than 0.05, R=0.6539). In the hippocampus, there was no correlation between SIRT3 levels and age. In human subjects with PD, SIRT3 was reduced by 56.8{+/-}15.5% and 34.0{+/-}5.6% in the SNc and hippocampus respectively regardless of age. Given that age is the primary risk factor for PD, this finding suggests that reduced SIRT3 may be a causative factor contributing to PD pathology. Next in human subjects with PD, we measured whether there was a correlation between the amount of aggregated alpha-synuclein and SIRT3 levels by measuring immunofluorescence of phosphorylated alpha-synuclein (p-syn), which is a marker for Lewy bodies. Interestingly, in the hippocampus, but not SNc, there was a positive correlation between SIRT3 and p-syn levels, despite p-syn being reduced compared to control. Next using an alpha-synuclein seeding rat model of PD, we assessed the disease-modifying effects of viral-mediated SIRT3 infusion. Six months following infusion of alpha-synuclein pre-formed fibrils (PFF) into the SNc, there was 38.8{+/-}4.5% loss of TH-positive neurons, impaired striatal dopamine metabolism and pathological alpha-synuclein throughout the brain. Phosphorylated-alpha-synuclein immunoreactivity was present in the SNc, olfactory tubercle, striatum, amygdala, hippocampus and motor cortex. In PD subjects, synuclein positive aggregates have also been reported in these brain regions. In PFF rats, infusion of rAAV1.SIRT3-myc in the SNc reduced abundance of alpha-synuclein inclusions in the SNc by 30.1{+/-}18.5% which was not seen when deacetylation deficient SIRT3H248Y was transduced. This demonstrates the importance of SIRT3 deacetylation in reducing alpha-synuclein aggregation. However, while SIRT3 transduction reduced aggregation in the SNc, it had no significant effect on phosphorylated-alpha-synuclein levels in other brain regions. These studies confirm that SIRT3 is directly correlated with senescence and aging in humans. We also provide evidence that reduced SIRT3 contributes to the pathology of clinical PD. Finally, by showing that over-expression of SIRT3 prevents alpha-synuclein aggregation through de-acetylation-dependent mechanisms, we further validate AAV1.SIRT3-myc as a potential disease-modifying therapy for PD. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Blane & Ashley Dallen & Melissa Oakley in Canada just raised over $10k together with two events. SynGAP Paddle Slap Stats: They had 12 teams play in the tournament.  About 120 people joined the crawfish boil.  Actual $ breakdown: Total Actual Income $23,250.00. Article https://www.localmemphis.com/article/life/family/rare-disease-research-promoted-integra[…]1-austim-epilepsy/522-b805046b-d05e-4f17-a8ab-69421293f926  Minnie's article in the Chicago Tribune. (behind firewall) https://www.chicagotribune.com/people/health/ct-hayden-cheng-syngap-diagnosis-0525-20230527-zacxfmtrhbd4bm5gbc3su5hsr4-story.html  Vicky & Paulina in Chihuahua, Mexico at Sociedad Mexicana de Neurología Pediátrica's annual conference https://twitter.com/cureSYNGAP1/status/1659250923611496449  Two blogs en Español https://www.syngapresearchfund.org/post/vacacionar-con-un-syngap1-147  https://www.syngapresearchfund.org/post/notas-de-terliz-mama-syngap1-145  STUDIES ENDD S1 NHS - Email ENDD@chop.edu to sign up and please cc mike@curesyngap1.org, lauren@curesyngap1.org & sydney@curesyngap1.org https://drive.google.com/file/d/1ASUkKQOgjbs9hkJVCJ40N8MbVFH4X9_h/view#  Watch #S10e105 https://www.youtube.com/watch?v=qy5YrPIlH0I  Cornell study English https://redcap.link/syngapcaregiversurvey  Spanish https://redcap.ctsc.weill.cornell.edu/redcap_protocols/surveys/?s=MWTW743PHENPPRPY  COMBINEDBrain Biorepository - https://www.syngapresearchfund.org/webinars/74-combinedbrain-biobank-our-partnership-with-srf-for-syngap1  SCIENCE 1st Syngap Patient Derived Models from SRF grant to Dr. Araki & Dr. Huganir https://www.biorxiv.org/content/10.1101/2023.05.25.542312v2  "Eye of the Fly" Chow article - https://www.ksl.com/article/50638506/eye-of-the-fly-how-fruit-flies-could-help-find-treatment-for-a-rare-genetic-disease  EVENTS June 10 - MDBR https://charity.pledgeit.org/t/Optdm6sOX9  June 21 - Splash for Syngap https://www.syngapresearchfund.org/post/share-your-love-for-someone-with-syngap1-for-splash4syngap  August 26 - Syngap Soiree  https://e.givesmart.com/events/wiH  October 7 - Scramble for Syngap https://secure.givelively.org/event/syngap-research-fund-incorporated/scramble-for-syngap-2023  October 21 - SynGAP Research Fund Gala Honoring Caren Leib - https://e.givesmart.com/events/wBy/  CONFERENCE Nov 30-Dec 1 - SYNGAP1 Conference 2023 hosted by SRF https://www.syngapresearchfund.org/professionals/syngap1-roundtable-2023-syngap-research-fund  Conference pre-registration link: https://Syngap.Fund/2023conf  Book hotels ASAP: https://Syngap.Fund/2023hotel Tshirts: https://www.bonfire.com/srf-syngap1-conference-2023/  WEBINARS June 8 - Therapeutic strategies for autism: Targeting Three levels of the central dogma of molecular biology - Dr. Lilia Iakoucheva & Mr. Derek Hong https://www.syngapresearchfund.org/webinars/78-therapeutic-strategies-for-autism-targeting[…]tral-dogma-of-molecular-biology-with-a-focus-on-syngap1  June 15 - Quantifying perturbed SYNGAP1 Function Caused by Coding Mutations - Dr. Michael Courtney from Turku in Finland https://www.syngapresearchfund.org/webinars/79-quantifying-perturbed-syngap1-function-caused-by-coding-mutations  PODS - Syngap Stories, interviews, see #8 with Heather Bensch https://www.syngapresearchfund.org/podcast-episodes/syngap1-stories-episode-008  - Syngap Stories, interviews, see #9 with Lauren Perry https://www.syngapresearchfund.org/podcast-episodes/syngap1-stories-episode-009  This is a podcast: subscribe to and rate this 10 minute #podcast #SYNGAP10 here  - https://www.syngapresearchfund.org/syngap10-podcast Apple podcasts:  https://podcasts.apple.com/us/podcast/syngap10-weekly-10-minute-updates-on-syngap1-video/id1560389818 Episode 106 of #Syngap10 - June 6, 2023 #epilepsy #autism #intellectualdisability #id #anxiety #raredisease #epilepsyawareness #autismawareness #rarediseaseresearch #SynGAPResearchFund #CareAboutRare #PatientAdvocacy #GCchat #Neurology #GeneChat --- Send in a voice message: https://podcasters.spotify.com/pod/show/syngap10/message

Blane & Ashley Dallen & Melissa Oakley in Canada just raised over $10k together with two events.   SynGAP Paddle Slap *this woman knows how to run a successful fundraising event with very low overhead! Stats: They had 12 teams play in the tournament.  About 120 people joined the crawfish boil.  Actual $ breakdown: Total Actual Income $23,250.00.   Article https://www.localmemphis.com/article/life/family/rare-disease-research-promoted-integra[…]1-austim-epilepsy/522-b805046b-d05e-4f17-a8ab-69421293f926    Minnie's article in the Chicago Tribune. (behind firewall) https://www.chicagotribune.com/people/health/ct-hayden-cheng-syngap-diagnosis-0525-20230527-zacxfmtrhbd4bm5gbc3su5hsr4-story.html    Vicky & Paulina in Chihuahua, Mexico at Sociedad Mexicana de Neurología Pediátrica's annual conference https://twitter.com/cureSYNGAP1/status/1659250923611496449    Two blogs en Español https://www.syngapresearchfund.org/post/vacacionar-con-un-syngap1-147  https://www.syngapresearchfund.org/post/notas-de-terliz-mama-syngap1-145    STUDIES ENDD S1 NHS - Email ENDD@chop.edu to sign up and please cc mike@curesyngap1.org, lauren@curesyngap1.org & sydney@curesyngap1.org https://drive.google.com/file/d/1ASUkKQOgjbs9hkJVCJ40N8MbVFH4X9_h/view#  Watch #S10e105 https://www.youtube.com/watch?v=qy5YrPIlH0I    Cornell study English https://redcap.link/syngapcaregiversurvey  Spanish https://redcap.ctsc.weill.cornell.edu/redcap_protocols/surveys/?s=MWTW743PHENPPRPY    COMBINEDBrain Biorepository - https://www.syngapresearchfund.org/webinars/74-combinedbrain-biobank-our-partnership-with-srf-for-syngap1    SCIENCE 1st Syngap Patient Derived Models from SRF grant to Dr. Araki & Dr. Huganir https://www.biorxiv.org/content/10.1101/2023.05.25.542312v2  "Eye of the Fly" Chow article - https://www.ksl.com/article/50638506/eye-of-the-fly-how-fruit-flies-could-help-find-treatment-for-a-rare-genetic-disease    EVENTS June 10 - MDBR https://charity.pledgeit.org/t/Optdm6sOX9    June 21 - Splash for Syngap https://www.syngapresearchfund.org/post/share-your-love-for-someone-with-syngap1-for-splash4syngap    August 26 - Syngap Soiree  https://e.givesmart.com/events/wiH    October 7 - Scramble for Syngap https://secure.givelively.org/event/syngap-research-fund-incorporated/scramble-for-syngap-2023    October 21 - SynGAP Research Fund Gala Honoring Caren Leib - https://e.givesmart.com/events/wBy/    CONFERENCE Nov 30-Dec 1 - SYNGAP1 Conference 2023 hosted by SynGAP Research Fund https://www.syngapresearchfund.org/professionals/syngap1-roundtable-2023-syngap-research-fund  Conference pre-registration link: https://Syngap.Fund/2023conf  Book hotels ASAP: https://Syngap.Fund/2023hotel Tshirts: https://www.bonfire.com/srf-syngap1-conference-2023/    WEBINARS June 8 - Therapeutic strategies for autism: Targeting Three levels of the central dogma of molecular biology - Dr. Lilia Iakoucheva & Mr. Derek Hong https://www.syngapresearchfund.org/webinars/78-therapeutic-strategies-for-autism-targeting[…]tral-dogma-of-molecular-biology-with-a-focus-on-syngap1    June 15 - Quantifying perturbed SYNGAP1 Function Caused by Coding Mutations - Dr. Michael Courtney from Turku in Finland https://www.syngapresearchfund.org/webinars/79-quantifying-perturbed-syngap1-function-caused-by-coding-mutations    Recently  - Dr. Baptiste Lacoste - Involvement of the brain endothelium in neurodevelopmental disorders https://www.syngapresearchfund.org/webinars/76-involvement-of-the-brain-endothelium-in-neurodevelopmental-disorders-syngap1  PODS - Syngap Stories, interviews, see #8 with Heather Bensch https://www.syngapresearchfund.org/podcast-episodes/syngap1-stories-episode-008  - Syngap Stories, interviews, see #9 with Lauren Perry https://www.syngapresearchfund.org/podcast-episodes/syngap1-stories-episode-009  Volunteer with SRF! Info@SyngapResearchFund.org    This is a podcast: subscribe to and rate this 10 minute #podcast #SYNGAP10 here  - https://www.syngapresearchfund.org/syngap10-podcast Apple podcasts:  https://podcasts.apple.com/us/podcast/syngap10-weekly-10-minute-updates-on-syngap1-video/id1560389818 Episode 106 of #Syngap10 - June 6, 2023 #epilepsy #autism #intellectualdisability #id #anxiety #raredisease #epilepsyawareness #autismawareness #rarediseaseresearch #SynGAPResearchFund #CareAboutRare #PatientAdvocacy #GCchat #Neurology #GeneChat

Bipolar Disorder has been listed as one of the leading disorders of the Global Burden of Diseases... Yet the amount of research and funding put towards it is abysmal. Laine and I share that during our clinical education, we were taught almost nothing about the experience of mania, diagnosing, or treating the disorders like Bipolar. This episode share's what we know so far (from the MANY articles Laine went through to try to make sense of it) and what's happening in the brain -- referencing studies from Harrison, Gettes, Tunbridge, Clark, Sahakian, and more. It also touches on what needs to be done to not only better support those who have experienced manic episodes or have been diagnosed, but what is required for the field of mental health to improve. The takeaways of this episode are some of our favorites -- you can hear it in Laine's voice at the end. Enjoy -- and as always, if you have any questions feel free to email us at info@brainblownpodcast.com. REFERENCES Dionisio et al. - "Cognitive flexibility impairment and reduced frontal cortex BDNF expression in the ouabain model of mania" Dzirasa et al. - "Impaired Limbic Gamma Oscillatory Synchrony during Anxiety-Related Behavior in a Genetic Mouse Model of Bipolar Mania" Ferrari et al. - "Depression and Mania Induce Pro-inflammatory Activation of Macrophages Following Application of Serum from Individuals with Bipolar Disorder" Schmidta et al. - "Cerebrospinal fluid hypocretin-1 (orexin A) levels in mania compared to unipolar depression and healthy controls" de Soussa et al. - "Lithium increases plasma brain-derived neurotrophic factor in acute bipolarmania: A preliminary 4-week study" Paul J. Harrison, John R. Geddes, and Elizabeth M. Tunbridge1 - "The Emerging Neurobiology of Bipolar Disorder" Luke Clark, Barbara J. Sahakian - "Cognitive neuroscience and brain imaging in bipolar disorder" G.S. Kirshenbaum, C. R. Burgess, N. De'ry, M. Fahnestock, J. H. Peever and J C Roder - "Attenuation of mania-like behavior in na+,k+-atpase a3 mutant mice by prospective therapies for bipolar disorder: melatonin and exercise" Emre Bora - "Neurocognitive features in clinical subgroups of bipolar disorder: A meta-analysis" Ryan W. Logan, Ph.D. and Colleen A. McClung, Ph.D. - "Animal Models of Bipolar Mania: The Past, Present and Future"

On this episode, I was joined by Marta New, the CEO of Radyus Research. Dr. New discusses: (0:00) Intro (1:37) Pre-Clinical Planning (7:15) What's the purpose of an IND? (14:10) Administration Route Selection (19:00) Candidate Selection and Animal Models (30:10) Pre-IND Meeting (44:00) IND Submissions and Approval Marta New PhD MBA is the CEO of Radyus Research. She is an experienced drug developer with a background in early-stage venture capital, considerable pharma R&D, and university technology transfer. 

Drs Madhukar Trivedi and Jeffrey Strawn discuss the impact of socioeconomic factors on outcomes of treatments in patients with major depressive disorder, including factors such as unemployment, race, sex, and age. Relevant disclosures can be found with the episode show notes on Medscape (https://www.medscape.com/viewarticle/984460). The topics and discussions are planned, produced, and reviewed independently of advertisers. This podcast is intended only for US healthcare professionals. Resources Depression https://emedicine.medscape.com/article/286759-overview Center for Clinical and Translational Science and Training (CCTST) https://www.cctst.org/ Socioeconomic Predictors of Treatment Outcomes Among Adults With Major Depressive Disorder https://pubmed.ncbi.nlm.nih.gov/35354325/ Cortisol and Major Depressive Disorder-Translating Findings From Humans to Animal Models and Back https://pubmed.ncbi.nlm.nih.gov/32038323/ Bayesian Hierarchical Models https://pubmed.ncbi.nlm.nih.gov/30535206/ The Impact of Age on Antidepressant Response: A Mega-Analysis of Individuals With Major Depressive Disorder https://pubmed.ncbi.nlm.nih.gov/36774767/ The Effectiveness of Individual Interpersonal Psychotherapy as a Treatment for Major Depressive Disorder in Adult Outpatients: A Systematic Review https://pubmed.ncbi.nlm.nih.gov/23312024/ Cognitive Behavioral Therapy for Depression https://emedicine.medscape.com/article/2094696-overview Depression and Psychodynamic Psychotherapy https://pubmed.ncbi.nlm.nih.gov/28614491/ Selective Serotonin Reuptake Inhibitors https://www.ncbi.nlm.nih.gov/books/NBK554406/ Cytochrome p450 Structure, Function and Clinical Significance: A Review https://pubmed.ncbi.nlm.nih.gov/28124606/  Optimizing Drug Selection in Psychopharmacology Based on 40 Significant CYP2C19- and CYP2D6-Biased Adverse Drug Reactions of Selective Serotonin Reuptake Inhibitors https://pubmed.ncbi.nlm.nih.gov/31616600/

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.24.537999v1?rss=1 Authors: Lisgaras, C. P., Scharfman, H. E. Abstract: Interictal spikes (IIS) are a common type of abnormal electrical activity in animal models of Alzheimers disease (AD) and AD patients. The brain regions where IIS are largest are not known but are important because such data would suggest sites that contribute to IIS generation. Because hippocampus and cortex exhibit altered excitability in AD models, we asked where IIS are largest along the cortical-CA1-dentate gyrus (DG) dorso-ventral axis. Because medial septal (MS) cholinergic neurons are overactive when IIS typically occur, we also tested the novel hypothesis that silencing the medial septohippocampal cholinergic neurons selectively would reduce IIS. We used 3 models of AD, Tg2576 mice, presenilin 2 knockout mice, and the Ts65Dn mouse model of Downs syndrome. To selectively silence MS cholinergic neurons, Tg2576 mice were bred with ChAT-Cre mice and offspring mice were injected in the MS with AAV encoding inhibitory designer receptors exclusively activated by designer drugs. We recorded EEG along the cortical-CA1-DG axis using silicon probes during wakefulness, slow-wave sleep (SWS) and rapid eye movement (REM) sleep. We detected IIS in all transgenic mice but not age-matched controls. IIS were detectable throughout the cortical-CA1-DG axis and were primarily during REM sleep. In all 3 models, IIS amplitudes were significantly greater in the DG granule cell layer vs. CA1 pyramidal layer or overlying cortex. Selective chemogenetic silencing of MS cholinergic neurons significantly reduced IIS frequency during REM sleep without affecting the overall duration or number of REM sleep bouts. Maximal IIS amplitude in the DG of 3 AD mouse models suggests that the DG could be one of the areas that contribute to IIS generation. Selectively reducing MS cholinergic tone could be a new strategy to reduce IIS in AD. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Dr. David G. Amaral (University of California, Davis) is an author of a review paper in the April issue of AJP looking at the use of animal models and other forms of translational neuroscience in the investigation of autism spectrum disorder.  He joins us on AJP Audio to discuss it.  Afterwards, we'll be joined once again by AJP Editor-in-Chief Dr. Ned Kalin to discuss the rest of the April issue.  Transcript   Amaral interview [00:56] Advantages and disadvantages of animal model research [02:14] What goes into determining which animals might be good candidates for research in human neurology? [04:52] How does basic research get translated into clinical treatments? [08:28] Alternatives to animal models [10:21] Promise of research moving forward [12:22] Kalin interview [15:30] Veenstra-VanderWeele et al. [15:46] Kato et al. [17:02] Zwicker et al. [19:17] Kim et al. [22:22] Zeng et al. [26:14] Be sure to let your colleagues know about the podcast, and please rate and review it on Apple Podcasts, Google Podcasts, Stitcher, Spotify, or wherever you listen to it. Subscribe to the podcast here. Listen to other podcasts produced by the American Psychiatric Association. Browse articles online. How authors may submit their work. Follow the journals of APA Publishing on Twitter. E-mail us at ajp@psych.org

How do research communities contend with controversial science? J. Benjamin Hurlbut, Ph.D., Arizona State University, Alysson Muotri, Ph.D., UC San Diego, Matthew Porteus, M.D., Ph.D., Stanford University, and Jacob (Yaqub) Hanna, M.D., Ph.D., Weizmann Institute of Science, explore controversial case studies and the limitations of scientific deliberation/dissent/ambivalence. Series: "Stem Cell Channel" [Health and Medicine] [Humanities] [Science] [Show ID: 38729]

How do research communities contend with controversial science? J. Benjamin Hurlbut, Ph.D., Arizona State University, Alysson Muotri, Ph.D., UC San Diego, Matthew Porteus, M.D., Ph.D., Stanford University, and Jacob (Yaqub) Hanna, M.D., Ph.D., Weizmann Institute of Science, explore controversial case studies and the limitations of scientific deliberation/dissent/ambivalence. Series: "Stem Cell Channel" [Health and Medicine] [Humanities] [Science] [Show ID: 38729]

How do research communities contend with controversial science? J. Benjamin Hurlbut, Ph.D., Arizona State University, Alysson Muotri, Ph.D., UC San Diego, Matthew Porteus, M.D., Ph.D., Stanford University, and Jacob (Yaqub) Hanna, M.D., Ph.D., Weizmann Institute of Science, explore controversial case studies and the limitations of scientific deliberation/dissent/ambivalence. Series: "Stem Cell Channel" [Health and Medicine] [Humanities] [Science] [Show ID: 38729]

How do research communities contend with controversial science? J. Benjamin Hurlbut, Ph.D., Arizona State University, Alysson Muotri, Ph.D., UC San Diego, Matthew Porteus, M.D., Ph.D., Stanford University, and Jacob (Yaqub) Hanna, M.D., Ph.D., Weizmann Institute of Science, explore controversial case studies and the limitations of scientific deliberation/dissent/ambivalence. Series: "Stem Cell Channel" [Health and Medicine] [Humanities] [Science] [Show ID: 38729]

How do research communities contend with controversial science? J. Benjamin Hurlbut, Ph.D., Arizona State University, Alysson Muotri, Ph.D., UC San Diego, Matthew Porteus, M.D., Ph.D., Stanford University, and Jacob (Yaqub) Hanna, M.D., Ph.D., Weizmann Institute of Science, explore controversial case studies and the limitations of scientific deliberation/dissent/ambivalence. Series: "Stem Cell Channel" [Health and Medicine] [Humanities] [Science] [Show ID: 38729]

How do research communities contend with controversial science? J. Benjamin Hurlbut, Ph.D., Arizona State University, Alysson Muotri, Ph.D., UC San Diego, Matthew Porteus, M.D., Ph.D., Stanford University, and Jacob (Yaqub) Hanna, M.D., Ph.D., Weizmann Institute of Science, explore controversial case studies and the limitations of scientific deliberation/dissent/ambivalence. Series: "Stem Cell Channel" [Health and Medicine] [Humanities] [Science] [Show ID: 38729]

How do research communities contend with controversial science? J. Benjamin Hurlbut, Ph.D., Arizona State University, Alysson Muotri, Ph.D., UC San Diego, Matthew Porteus, M.D., Ph.D., Stanford University, and Jacob (Yaqub) Hanna, M.D., Ph.D., Weizmann Institute of Science, explore controversial case studies and the limitations of scientific deliberation/dissent/ambivalence. Series: "Stem Cell Channel" [Health and Medicine] [Humanities] [Science] [Show ID: 38729]

How do research communities contend with controversial science? J. Benjamin Hurlbut, Ph.D., Arizona State University, Alysson Muotri, Ph.D., UC San Diego, Matthew Porteus, M.D., Ph.D., Stanford University, and Jacob (Yaqub) Hanna, M.D., Ph.D., Weizmann Institute of Science, explore controversial case studies and the limitations of scientific deliberation/dissent/ambivalence. Series: "Stem Cell Channel" [Health and Medicine] [Humanities] [Science] [Show ID: 38729]

Just like no two people are the same, no two strains of mice are the same. Using dozens of different strains of mice with and without a genetic mutation associated with autism called CHD8, researchers at University of Southern California showed great variability in the effect of this mutation on behaviors associated with neurodevelopmental disorders. … Continue reading "Animal models can explain heterogeneity"

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.06.519361v1?rss=1 Authors: Broeren, B. O., Hundepool, C. A., Kumas, A. H., Duraku, L. S., Walbeehm, E. T., Hooijmans, C. R., Power, D. M., Zuidam, J. M., De Jong, T. Abstract: Background: Treatment of nerve injuries proves to be a worldwide clinical challenge. Acellular nerve allografts are suggested to be a promising alternative for bridging a nerve gap to the current gold standard, an autologous nerve graft. Objective: To systematically review the efficacy of the acellular nerve allograft, its difference from the gold standard (the nerve autograft) and to discuss its possible indications. Material and methods: PubMed, Embase and Web of Science were systematically searched until the 4th of January 2022. Original peer reviewed paper that presented 1) distinctive data; 2) a clear comparison between not immunologically processed acellular allografts and autologous nerve transfers; 3) was performed in laboratory animals of all species and sex. Meta analyses and subgroup analyses (for graft length and species) were conducted for muscle weight, sciatic function index, ankle angle, nerve conduction velocity, axon count diameter, tetanic contraction and amplitude using a Random effects model. Subgroup analyses were conducted on graft length and species. Results: Fifty articles were included in this review and all were included in the meta-analyses. An acellular allograft resulted in a significantly lower muscle weight, sciatic function index, ankle angle, nerve conduction velocity, axon count and smaller diameter, tetanic contraction compared to an autologous nerve graft. No difference was found in amplitude between acellular allografts and autologous nerve transfers. Post hoc subgroup analyses of graft length showed a significant reduced muscle weight in long grafts versus small and medium length grafts. All included studies showed a large variance in methodological design. Conclusion: Our review shows that the included studies, investigating the use of acellular allografts, showed a large variance in methodological design and are as a consequence difficult to compare. Nevertheless, our results indicate that treating a nerve gap with an allograft results in an inferior nerve recovery compared to an autograft in seven out of eight outcomes assessed in experimental animals. In addition, based on our preliminary post hoc subgroup analyses we suggest that when an allograft is being used an allograft in short and medium (0-1cm, greater than 1-2cm) nerve gaps is preferred over an allograft in long ( greater than 2cm) nerve gaps. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.09.20.508692v1?rss=1 Authors: Lopez-Rodriguez, A. B., Murray, C., Kealy, J., Towns, C., Nazmi, A., Arnold, L., Doran, M., Lowry, J., Cunningham, C. Abstract: Autism Spectrum Disorders (ASD) are predominantly developmental in nature and largely genetically determined. There are some human data supporting the idea that fever can improve symptoms in some individuals but the human data for this are limited and there are almost no data to support this from animal models. In the current study, we used a whole body hyperthermia (WBH) protocol and systemic inflammation induced by bacterial endotoxin (LPS) to dissociate temperature and inflammatory elements of fever in order to examine the impact of these environmental stressors on behavioural signs in two animal models relevant to ASD: C58BL/6 and Shank3B- mice. While only LPS induced inflammatory signatures in the brain, WBH and LPS induced both overlapping and distinct neuronal cFos activation in several brain regions and modest effects on heat shock gene expression. In behavioural experiments LPS significantly suppressed most activities over 24-48 hours while WBH reduced repetitive behaviours and improved social interaction in C58BL/6 mice. In Shank3B- mice WBH significantly reduced compulsive grooming. The data are the first, to our knowledge, to demonstrate that elevated body temperature, in the absence of underpinning inflammation, can improve some behavioural signs in two distinct animal models of ASD. Given the developmental and genetic nature of ASD, evidence that symptoms may be ameliorated by environmental perturbations indicates that there are possibilities for improving function in these individuals. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer

The avarice of the human species for our health and welfare alone can truly shock and horrify at times. As it should. So that the visceral feeling of Animal abuse for our benefit is a catalyst for change.https://www.cnn.com/2022/08/10/us/experiment-beagles-rescued-scli-intl/index.htmlhttps://news.northeastern.edu/2022/07/21/beagles-lab-testing/#:~:text=Among%20the%20dogs%20that%20are,likely%20use%20them%20as%20well.

AMiNDR is back and excited to bring you more literature on Alzheimer's Disease. In this episode, we've got papers published in May of 2022 on the subject of changes to synaptic transmission and neuronal excitability. Anusha covers subjects like calcium homeostasis, synaptic function, and how to translate findings to humans and human models, so join her if your neurons are excited by the topic!  Sections in this episode: Calcium Homeostasis (2:54) Synaptic Function in Animal Models (5:26) Human Models (10:28)  -------------------------------------------------------------- To find the numbered bibliography with all the papers covered in this episode, click here, or use the link below: https://drive.google.com/file/d/1cC1rtUbyo1PgJOlQWISW4Eccnie4qada/view To access the folder with ALL our bibliographies, follow this link (it will be updated as we publish episodes and process bibliographies), or use the link below: https://drive.google.com/drive/folders/1bzSzkY9ZHzzY8Xhzt0HZfZhRG1Gq_Si-?usp=sharing You can also find all of our bibliographies on our website: www.amindr.com. -------------------------------------------------------------- Follow-up on social media for more updates! Twitter: @AMiNDR_podcast Instagram: @AMiNDR.podcast Facebook:  AMiNDR Youtube: AMiNDR Podcast LinkedIn: AMiNDR Podcast Email: amindrpodcast@gmail.com -------------------------------------------------------------- Please help us spread the word about AMiNDR to your friends, colleagues, and networks! And if you could leave us a rating and/or review on your streaming app of choice (Apple Podcasts, Spotify, or wherever you listen to the podcast), that would be greatly appreciated! It helps us a lot and we thank you in advance for leaving a review! Don't forget to subscribe to hear about new episodes as they come out too. Thank you to our sponsor, the Canadian Consortium of Neurodegeneration in Aging, or CCNA, for their financial support of this podcast. This helps us to stay on the air and bring you high quality episodes. You can find out more about the CCNA on their website: https://ccna-ccnv.ca/. Our team of volunteers works tirelessly each month to bring you every episode of AMiNDR. This episode was scripted, hosted and edited by Anusha Kamesh and reviewed by Sarah Louadi and Judy Cheng. The bibliography and wordcloud were created by Lara Onbasi (www.wordart.com). Big thanks to the sorting team for taking on the enormous task of sorting all of the Alzheimer's Disease papers into episodes each month. For May 2022, the sorters were Sarah Louadi, Christy Yu, Ben Cornish, Eden Dubchak, Kira Tosefsky, Elyn Rowe, and Ellen Koch. Also, props to our management team, which includes Sarah Louadi, Ellen Koch, Naila Kuhlmann, Elyn Rowe, Anusha Kamesh, and Lara Onbasi for keeping everything running smoothly.  Our music is from "Journey of a Neurotransmitter" by musician and fellow neuroscientist Anusha Kamesh; you can find the original piece and her other music on soundcloud under Anusha Kamesh or on her YouTube channel, AKMusic. https://www.youtube.com/channel/UCMH7chrAdtCUZuGia16FR4w -------------------------------------------------------------- If you are interested in joining the team, send us your CV by email. We are specifically looking for help with sorting abstracts by topic, abstract summaries and hosting, audio editing, creating bibliographies, and outreach/marketing. However, if you are interested in helping in other ways, don't hesitate to apply anyways. -------------------------------------------------------------- *About AMiNDR: * Learn more about this project and the team behind it by listening to our first episode: "Welcome to AMiNDR!"

In this episode, Karl Friston (director of the Max Planck Institute for Human Cognitive and Brain Sciences) discusses the animal model of degenerative disease and its relevance to human pathology. He talks about the use of rodent models to study chemotherapeutics, and highlights some of the pitfalls of this research.

Dr. Gregory Dussor is Professor and Chair of the Department of Neuroscience at the University of Texas at Dallas. His work focuses on understanding how the sensory innervation of the meninges contributes to headache disorders. Using several preclinical models, his group has identified numerous targets within this afferent nociceptive system including several that may contribute to sex differences observed in migraine.  In this Migraine Science Collaborative podcast, Dussor speaks with MSC Executive Editor Neil Andrews to discuss his path to studying migraine, his research contributions so far – especially his work to develop better animal models of migraine – what's going well in the migraine field and what needs to get better –  and even his love of coffee and the band Phish. 

In this weeks episode, Han is joined by PhD candidate Melinda Karth. Melinda is a PhD candidate at Purdue University, where she is looking at anxiety in individuals "recovered" from anorexia nervosa.With Melinda, we begin discussing her journey into neuroscience, and what inspired her research. We then speak about the current animal models that are used in eating disorder research, including the binge eating model and anorexia model in mice. We also discuss the potential for a bulimia nervosa animal model, and PICA in giraffes!We then speak about Melinda's PhD work, and discuss how animals demonstrate symptoms of anxiety and depression, and discuss her PhD looking at anxiety and anorexia in weight restored individuals. Finally, we discuss how different parts of the brain are involved in symptoms of eating disorders and anxiety. To find out more about Melinda and her research, you can follow her @MelindaKarth and check out Melinda's blogs here: https://www.psychologytoday.com/us/blog/the-neuroscience-eating-disordersPlease note we discuss a number of eating disorder behaviours and how they are manipulated in mice models. Take care and tread lightly.

The average cost of developing a new drug is estimated at over $2 billion. Roughly 10% of pre-clinical drugs ever make it to human trials. And each year, $50 billion is “misspent” in the trial & error method of research and development. An AI-enabled “decision engine” could help researchers find cures to rare diseases, bridge the translational gap between animal models to human systems, and move faster in drug development reducing associated R&D costs. Today on the show we chat with Jo Varshney, the founder of VeriSIM Life, about the AI-enabled technology that is cutting the time for drug development in half. Searching for a drug candidate for bone cancer led Dr. Varshney to tackle the challenges of better predicting outcomes, improving methods for drug discovery, and building models closer to human systems.About Jo Varshney and VeriSIM LifeDr. Jo Varshney is a multi-disciplinary and celebrated leader in veterinary & human health development. She is the founder and CEO of VeriSIM Life, which is building AI-enabled biosimulation technology to empower researchers to predict how potential drug candidates will interact in animal models. Dr. Varshney holds a Ph.D. in Comparative Oncology and Genomics from the University of Minnesota, a Master's Degree in Translational Pathobiology & Bioinformatics from Penn State University, and a Doctorate of Veterinary Medicine from the College of Veterinary Science & Animal Husbandry. She serves as a Scientific Advisor at SVAI, a San Francisco-based non-profit organization promoting education and cooperative research at the intersection of computational and life sciences. Links: VeriSIM Life LinkedIn | Jo VarshneyGenomics HackathonWikipedia | Drug DiscoveryWikipedia | The Translational GapQualio WebsitePrevious episodes: https://www.qualio.com/from-lab-to-launch-podcastApply to be on the show: https://forms.gle/uUH2YtCFxJHrVGeL8Music by keldez

This month on Episode 36 of Discover CircRes, host Cynthia St. Hilaire highlights original research articles featured in the April 29 and May 13 issues of Circulation Research. This episode also features a conversation with Dr Patricia Nguyen and Jessica D'Addabbo from Stanford University about their study, Human Coronary Plaque T-cells are Clonal and Cross-React to Virus and Self.   Article highlights:   Zanoli, et al. COVID-19 and Vascular Aging   Wang, et al. JP2NT Gene Therapy in a Mouse Heart Failure Mode   Harraz, et al. Piezo1 Is a Mechanosensor in CNS Capillaries   Zhao, et al. BAT sEVs in Exercise Cardioprotection   Cindy St. Hilaire:        Hi, and welcome to Discover CircRes, the podcast of the American Heart Association's journal, Circulation Research. I'm your host, Dr Cyndy St. Hilaire, from the Vascular Medicine Institute at the University of Pittsburgh. And today, I'll be highlighting the articles from our April 29th and May 13th issues of Circulation Research. I also will speak with Dr Patricia Nguyen and Jessica D'Addabbo from Stanford University about their study, Human Coronary Plaque T-cells are Clonal and Cross-React to Virus and Self.   Cindy St. Hilaire:        The first article I want to share is titled Vascular Dysfunction of COVID 19 Is Partially Reverted in the Long-Term. The first author is Agostino Gaudio and the corresponding author is Luca Zanoli. And they're from the University of Catania. Cardiovascular complications, such as endothelial dysfunction, arterial stiffness, thrombosis and heart disease are common in COVID 19. But how quickly such issues resolve, once the acute phase of the illness has passed, remains unclear. To find out, this group examined aortic and brachial pulse wave velocity, and other measures of arterial stiffness in 90 people who, several months earlier, had been hospitalized with COVID 19. These measurements were compared with data from 180 controls, matched for age, sex, ethnicity and body mass index, whose arterial stiffness had been assessed prior to the pandemic. 41 of the COVID patients were also examined 27 weeks later to assess any changes in arterial stiffness over time. Together, the data showed arterial stiffness was higher in COVID patients than in controls. And though it improved over time, it tended to remain higher than normal for almost a year after COVID.   Cindy St. Hilaire:        This finding could suggest residual structural damage to the arterial walls or possibly, persistent low-grade inflammation in COVID patients. Either way, since arterial stiffness is a predictor of cardiovascular health, its potential longterm effects in COVID patients deserves further longitudinal studies.   Cindy St. Hilaire:        The second article I want to share is titled Gene Therapy with the N-Terminus of Junctophilin-2 Improves Heart Failure in Mice. The first author is Jinxi Wang and the corresponding author is Long-Sheng Song from the University of Iowa. Junctophilin-2 is a protein with a split personality. Normally, it forms part of the heart's excitation contraction coupling machinery. But when the heart is stressed, JP2 literally splits in two, and sends its N-terminal domain, JP2NT, to the nucleus, where it suppresses transcription of genes involved in fibrosis, hypertrophy, inflammation and other heart failure related processes. However, if this stress is severe or sustained, the protective action of JP2NT is insufficient to halt the progressive failure. This group asked. "What if this N-terminal domain could be ramped up using gene therapy to aid a failing mouse heart?"   Cindy St. Hilaire:        To answer this question, they injected adenoviral vectors encoding JP2NT into mice either before or soon after transaortic constriction, or TAC, tack, which is a method of experimentally inducing heart failure. They found, in both cases, that the injected animals fared better than the controls. Animals injected before TAC showed less severe cardiac remodeling than control mice, while those treated soon after TAC exhibited slower loss of heart function with reduced ventricle dilation and fibrosis. These data suggest that supplementing JP2NT, via gene therapy or other means, could be a promising strategy for treating heart failure. And this data provides a basis for future translational studies.   Cindy St. Hilaire:        The third article I want to share is titled Piezo1 Is a Mechanosensor Channel in Central Nervous System Capillaries. The first and corresponding author is Osama Harraz from the University of Vermont. Neurovascular coupling is the process whereby transient activation of neurons leads to an upsurge in local blood flow to accommodate the increased metabolic needs of the cell. It's known that agents released from active neurons trigger changes in local capillaries that prompt vasodilation, but how these hemodynamic changes are sensed and controlled is not entirely clear. This group suspected that the mechanosensory protein Piezo1, a calcium channel that regulates dilation and constriction of other blood vessels, may be involved. But whether Piezo1 is even found in the microcirculation of the CNS was unknown. This group shows that Piezo1 is present in cortical capillaries of the brain and the retina of the mouse, and that it responds to changes in blood pressure and flow.   Cindy St. Hilaire:        Ex vivo preparations of mouse retina showed that experimentally induced changes in hemodynamics caused calcium transients and related currents within capillary endothelial cells, and that these were dependent on the presence of Piezo1. While it is not entirely clear how Piezo1 influences cerebral blood flow, its pressure induced activation of CNS capillary endothelial cells suggest a critical role in neurovascular coupling.   Cindy St. Hilaire:        The last article I want to share is titled Small Extracellular Vesicles from Brown Adipose Tissue Mediate Exercise Cardioprotection. The first authors are Hang Zhao and Xiyao Chen. And the corresponding authors are Fuyang Zhang and Ling Tao from the Fourth Military Medical University. Regular aerobic exercise is good for the heart and it increases the body's proportion of brown adipose tissue relative to white adipose tissue. This link has led to the idea that brown fat, possibly via its endocrinal activity, might somehow contribute to exercise related cardioprotection. Zhao and colleagues now show that, indeed, brown fat produces extracellular vesicles that are key to preserving heart health. While mice subjected to four weeks of aerobic exercise were better protected against subsequent heart injury than their sedentary counterparts, blocking the production of EVs prior to exercise significantly impaired this protection. Furthermore, injection of brown fat derived EVs into the hearts of mice lessened the impact of subsequent cardiac injury.   Cindy St. Hilaire:        The team went on to identify micro RNAs within the vesicles responsible for this protection, showing that the micro RNAs suppressed an apoptosis pathway in cardiomyocytes. In identifying mechanisms and molecules involved in exercise related cardio protection, the work will inform the development of exercise mimicking treatments for people at risk of heart disease or who are intolerant to exercise.   Cindy St. Hilaire:        Lastly, I want to bring up that the April 29th issue of Circulation Research also contains a short Review Series on pulmonary hypertension, with articles on: The Latest in Animal Models of Pulmonary Hypertension and Right Ventricular Failure, by Olivier Boucherat; Harnessing Big Data to Advance Treatment and Understanding of Pulmonary Hypertension, by Christopher Rhodes and colleagues; New Mutations and Pathogenesis of Pulmonary Hypertension: Progress and Puzzles in Disease Pathogenesis, by Christophe Guignabert and colleagues; Group 3 Pulmonary Hypertension From Bench to Bedside, by Corey Ventetuolo and colleagues; and Novel Approaches to Imaging the Pulmonary Vasculature and Right Heart, by Sudarshan Rajagopal and colleagues; and Understanding the Pathobiology of Pulmonary Hypertension Due to Left Heart Disease, by Jessica Huston and colleagues.   Cindy St. Hilaire:        Today, Dr Patricia Nguyen and Jessica D'Addabbo, from Sanford University, are with me to discuss their study, Human Coronary Plaque T-cells are Clonal and Cross-React to Virus and Self. And this article is in our May 13th issue of Circulation Research. So, Trisha and Jessica, thank you so much for joining me today.   Jessica D'Addabbo:    Thank you for having us.   Patricia Nguyen:         Yes. Thank you for inviting us to your podcast. We're very excited to be here.   Cindy St. Hilaire:        Yeah. And I know there's lots of authors involved in this study, so unfortunately we can't have everyone join us, but I appreciate you all taking the time.   Patricia Nguyen:         This is like a humongous effort by many people in the group, including Roshni Roy Chowdhury, and Xianxi Huang, as well as Charles Chan and Mark Davis. So, we thank you.   Cindy St. Hilaire:        So atherosclerosis, it stems from lipid deposition in the vascular wall. And that lipid deposition causes a whole bunch of things to happen that lead to a chronic inflammatory state. And there's many cells that can be inflammatory. And this study, your study, is really focusing on the role of T-cells in the atherosclerotic plaque. So, before we get into the nitty gritty details of your study, can you share with us, what is it that a T-cell does normally and what is it doing in a plaque? Or rather, let me rephrase that as, what did we know a T-cell was doing in a plaque before your study?   Patricia Nguyen:         So, T-cells, as you know, are members of the adaptive immune system. They are the master regulators of the entire immune system, secreting cytokines and other proteins to attract immune cells to a diseased portion of the body, for example. T-cells have been characterized in plaque previously, mainly with immunohisto chemistry. And their characterization has also been recently performed using single cell technologies. Those studies have been restricted to mainly mirroring studies, studies in mice in their aortic walls, in addition to human carotid arteries. So, it is well known that T cells are found in plaque and a lot of attention has been given to the macrophage subset as the innate immune D. But let's not forget the T-cell because they're actually composed about... 50% in the plaque are T-cells.   Patricia Nguyen:         And we were particularly interested in the T-cell population because we have a strong collaboration with Dr Mark Davis, who's actually the pioneer of T-cell biology and was the first to describe the T-cell receptor alpha beta receptor in his lab in the 1970s. So, he has developed many techniques to interrogate T-cell biology. And our collaboration with him has allowed us and enabled us to perform many of these single cell technologies. In addition, his colleague, Dr Chen, also was pivotal in helping us with the interrogation and understanding of the T-cells in plaque.   Cindy St. Hilaire:        And I think one of the really neat strengths of your study is that you used human coronary artery plaques. So, could you walk us through? What was that like? I collect a lot of human tissue in my lab. I get a lot of aortic valves from the clinic. And it's a lot of logistics. And a lot of times, we're just fixing them, but you are not just fixing them. So, can you walk us through? What was that experimental process from the patient to the Petri dish? And also, could you tell us a little bit about your patient population that you sampled from?   Jessica D'Addabbo:    So, these were coronary arteries that we got from patients receiving a heart transplant. So, they were getting a heart transplant for various reasons, and we would receive their old heart, and someone would help us dissect out the coronary arteries from these. And then, we would process each of these coronary arteries separately. And this happened at whatever hour the hearts came out of the patient.   Jessica D'Addabbo:    So sometime, I was coming in at 3:00 AM with Dr Nguyen and we would be working on these hearts then, because we wanted the samples to be as fresh as possible. So, we would get the arteries. We would digest out the tissue. And then, we would have certain staining profiles that we wanted to look at so that we could put the cells on fax to be able to sort the cells, and then do all the downstream sequencing from there.   Cindy St. Hilaire:        So, in terms of, I don't know, the time when you get that phone call that a heart's coming in to actually getting those single cells that you can either send a fax or send a sequencing, how long did that take, on a good day? Let's talk only about good days.   Jessica D'Addabbo:    Yeah. A lot of factors went into that, sometimes depending on availability of things. But usually, we were ready with all of the materials in advance. So, I'd say it could be anywhere from six to 12 hours, it would take, to get everything sorted. Then, everything after that would happen. But that was just that critical period of making sure we got the cells fresh.   Patricia Nguyen:         So we have to credit the CT surgeons at Stanford for setting up the program or the structure, infrastructure, that enables us to obtain this precious tissue. That is Jack Boyd and Joseph Woo of CT surgery. So, they have enabled human research on hearts by making these tissues available. Because as you know, a transplant... They can say the transplant's happening at 12:00 AM, but it actually doesn't happen until 4:00 AM. And I think it's very difficult for a lab to make that happen all the time. And I think having their support in this paper was critical. And this has allowed us, enabled us, to interrogate kind of the spectrum of disease, especially focusing on T-cells, which are... They make a portion of the plaque, but the plaque itself has not like a million cells that are immune. A lot of them are not immune. So, enabling us to get the tissue in a timely fashion where they're not out of the body for more than 30 minutes enables us to interrogate these small populations of cells.   Cindy St. Hilaire:        That's actually the perfect segue to my next question, which is, how many cells in a plaque were you able to investigate with the single cell analysis? And what was the percentage again of the T-cells in those plaques or in... I guess you looked at different phases of plaque. So, what was that spectrum for the percentage of T-cells?   Patricia Nguyen:         So, for 10X, for example, you need a minimum of 10,000 captured cells. You could do less, but the utility of the 10X is maximized with 10,000. So, many times before the ability to multiplex these tissues, we were doing like capturing 5,000 for example. And the number of cells follows kind of the disease progression, in the sense that as a disease is more severe, you have more immune cells, in general. And it kind of decreases as it becomes more fibrotic and scarred, like calcified. So, it was a bit challenging to get very early just lipid-only cells. And a lot of those, we captured like 3000 or something like that. And efficiency is like 80% perhaps. So, you kind of capture…   Cindy St. Hilaire:        And also, how many excised hearts are going to have early athero? So, it's...   Patricia Nguyen:         Well, there are... nonischemics will have...   Cindy St. Hilaire:        Oh, okay. Okay.   Patricia Nguyen:         So, the range was nonischemic to ischemic.   Cindy St. Hilaire:        Oh great.   Patricia Nguyen:         So, about a portion... I would say one third of the total heart transplants were ischemic. And a lot of them were non ischemic. But as you know, the nonischemic can mix with ischemia. And so, they could have mild to moderate disease in the other arteries, for example, but not severe like 70%/90% obstruction.   Cindy St. Hilaire:        Wow. That's so great. That's amazing. Amazing sample size you have. So T-cell, it's kind of an umbrella term, right? There's many different types of T-cells. And when you start to get in the nitty gritty, they really do have distinct functions. So, what types of T-cells did you see and did you focus on in this study?   Jessica D'Addabbo:    So, the two main types of T-cells are CD4 positive T-cells and CD8 positive T-cells. And we looked at both of these T-cells from patients. We usually sorted multiple plates from each. And then, with 10X, we captured both. But our major finding was actually that the CD8 positive t-cell population was more clonally expanded than the CD4 population, which led us to believe that these cells were more important in the coronary artery disease progression and in the study that we were doing because for a cell to be clonally expanded, it means it was previously exposed to an antigen. And so, if we're finding these T-cells that are clonally expanded in our plaques, then we're hypothesizing that they were likely exposed to some sort of antigen, and then expanded, and then settled into the plaque.   Cindy St. Hilaire:        And when you're saying expansion, are you talking about them being exposed to the antigen in the plaque and expanding there? Or do you think they're being triggered in the periphery and then honing in as a more clonal population?   Patricia Nguyen:         So, that's a great question. And unfortunately, I don't have the answer to that. So basically-   Jessica D'Addabbo:    Next paper, next paper.   Patricia Nguyen:         Exactly. So, we... Interesting to expand on Jessica's answer. Predominantly what was found, as you said, was memory T-cells, so memory T-cells expressing specific markers, so memory versus naive. And these were effector T-cells. And memory meaning they were previously expanded by antigen engagement, and just happened to be in the plaque for whatever reason. We do not know why T-cells specifically are attracted to the plaque, but they are obviously there. And they're in a memory state, if you will. And some of them did display activation markers, which suggested that they clonally expanded to an antigen. What that antigen is, is the topic of another paper. But certainly, it is important to understand that these patients that we recruit, because they were transplant patients, they're not actively infected, right? That is a exclusionary criteria for transplants, right?   Patricia Nguyen:         So, that means these T-cells were there for unclear reasons. Why they're there is unclear. Whether they are your resident T-cells also is unclear, because the definition of resident T-cell still remains controversial. And you actually have to do lineage tracking studies to find out, "Okay, where... Did they come from the bone marrow? Did they come from the periphery? How did they get there?" Versus, "Okay. They were already there and they just expanded, for whatever reason, inside the plaque."   Cindy St. Hilaire:        So, your title... It was a great title, with this provocative statement, "T-cells are clonal and cross react to virus and self." So, tell us a little bit more about this react to virus and self bit. What did your data show?   Jessica D'Addabbo:    So, because of the way we sequenced the T-cell receptor, we were able to have paired alpha and beta chains. And because we knew the HLA type of the patients, we were able to put the sequences that we got out after we sequenced these through an algorithm called GLIPH, which allows us to look at the CDR3 region of the T cell receptor, which is the epitope binding region. And there are certain peptide. They're about anywhere from three to four amino acids long. These are mapped to certain binding specificities to known peptides. And so, basically, we were able to look at which epitopes were most common in our plaques. And we found that after comparing these to other epitopes, that these were actually more binding to virus. Patricia Nguyen:         So let me add to what Jessica stated, and kind of emphasize the value of the data set, if you will. So, this is, I believe, the first study that provides the complete TCR repertoire of coronary plaque, and actually any plaque that I know of, which is special because we know that there is specificity of TCR binding. It's more complicated than the antibody that binds directly from B cells to the antigen, because the T-cells bind processed antigen. So, the antigens are processed by antigen presenting cells like Dendritic cells and macrophages. And they have a specific HLA MHC class that they need to present to. And they need both arms, the antigen epitope and the MHC, to activate the T-cell. So unfortunately, it's not very direct to find the antigen that is actually activating the T-cell because we're only given a piece of it. Right?            Patricia Nguyen:         But we have provided a comprehensive map of all the TCRs that we find in the plaque. And these TCRs have a sequence, an immuno acid sequence. And luckily, in the literature, there is a database of all TCR specificities. Okay. So, armed with our TCR repertoire, we can then match our TCR repertoire with an existing database of known TCR specificities. Surprisingly, the matching TCRs are specific to virus, like flu, EBV and CMB. And also, because this was done in the era of COVID, we thought it would be important to look at the coronavirus database. We did find that there were matches to the coronavirus database. Even though our finding is not specific to SARS, it does lend to some potential mechanistic link there as well.   So, because this is all computational, it is important to validate. So, the importance of validation requires us to put the TCR alpha beta chain into a Jurkat cell, which is a T-cell line that does not have alpha beta chains on it, and then expose it to what we think is the cognate antigen epitote, with the corresponding HLA MHC APC. Because you don't have all those pieces, it will not work. Yes. So importantly, we did find that what we predicted to have the specificity of a flu peptide had specificity to a flu peptide.   Patricia Nguyen:         So then, the important question was, "Okay, these patients aren't infected, right? Why are these things here? Is there a potential cross reactivity with self peptides?"   Patricia Nguyen:         So luckily, our collaborator, Dr Charles Chan, was able to connect us with another computational algorithm that he was familiar with, whereby we were able to take the peptide sequences from the flu and match them with peptide sequencing from proteins that are self and ubiquitous. And we demonstrated, again, these T-cells were activated in vitro. That is why we concluded that there's a potential cross reactivity between self and virus that can potentially lead to thrombosis associated with viral infections. Of course, this all needs to be proved in vivo.   Cindy St. Hilaire:        Sure, sure.   Patricia Nguyen:         It's that first step for other things.   Cindy St. Hilaire:        The other big immune cell that we know is in atherosclerotic plaques and that's macrophages. And they can help to present antigens and things like that. And they also help to chew up the necrotic bits. And so, do you think that this T-cell component is an earlier, maybe disease driving, process or an adaptive process that goes awry as a secondary event? Patricia Nguyen:         So, I'm a fan of the T-cell. So... I'm with team T cell. I would like to think that it is playing an active role in pathology in this case and not a reactive role, in the sense of just being there. I think that the T-cell is actively communicating with other cells within the plaque, and promoting pro fibrotic and pro inflammatory reactions, depending on the T-cell. So, a subset of this paper was looking at kind of the interactions between the T-cell and other cells within the plaque, like macrophages and smooth muscle cells. And as we know, T-cells are activated and they produce cytokines. Those cytokines then communicate to other cells. And we found that, computationally, when you look at the transcriptome, there is a pro-inflammatory signature of the T-cell that resides in the more complex stage. And then, there's an anti-inflammatory signature that kind of resides in the transition between lipid and fibro atheroma, if you will.   Cindy St. Hilaire:        So, do you know, or is it known, how dynamic these populations are? Obviously, the hearts that you got, the samples you got, didn't have active infections. But do you know perhaps even how long ago they happened, or even how soon after there might be an infection or an antigen presented that you could get this expansion? And could that be a real driver of rupture or thrombosis?   Patricia Nguyen:         So, in theory, you would suppose that T-cells expanding and dividing and producing more and more cytokines would then lead to more macrophages coming, more of their production of proteinases that destroy the plaque. Right? So yes, in theory, yes. I think it's very difficult to kind of map the progression of T cell clonality in the current model that we have, because we're just collecting tissues. However, in the future, as organoids become more in science and kind of a primary tissue, where we can... For example, Mark Davis is making organoids with spleen, and also introducing skin to that.   Patricia Nguyen:         And certainly, we could think of an organoid involving the vasculature with immune cells introduced. And so, I think, in the next phase, project 2.0, we can investigate what... like over time, if you could model atherosclerosis and the immune system contribution, T-cells as well as macrophages and other immune cells, you can then kind of map how it happens in humans. Because obviously, mice are different. We know that mice... Actually, the models of transgenic mice do not rupture. It's very hard to make them rupture. Right?   Cindy St. Hilaire:        Well, if you stop feeding them high fat diet, the plaque goes away.   Patricia Nguyen:         For sure, for sure. So I think.. I mean, Mark Davis is a huge proponent of human based research, like research on human tissue. And as a physician scientist, obviously I'm more inclined to do human based research. And Jessica's going to be a physician someday soon. And I'm sure she's more inclined to do human based research. And certainly, the mouse model and in vitro models are great because you can manipulate them. But ultimately, we are trying to cure human diseases.   Cindy St. Hilaire:        Mice are not little humans. That's what we say in my lab. I similarly do a lot of human based stuff and it's amazing how great mice are for certain things, but still how much is not there when we need to really fully recapitulate a disease model.   So, my last question is kind of regarding this autoimmune angle of your findings. And that is, women tend to have more autoimmune diseases than men, but due to the fact that you are getting heart transplants, you've got a whole lot more men in your study than women. I think it was like 31 men to four women. But, I mean, what can you do? It's the nature of heart transplants. But I'm wondering, did you happen to notice...Maybe the sample size perhaps is too small, but were there any differences in the populations of these cells between women and men? And do you think there could be any differences regarding this more prevalence of autoimmune like reactions in women?   Patricia Nguyen:         So, that's an interesting question, but you hit it on the nose when you said "Your sample is defined mainly by men." And in addition, the samples that were women tend to have less disease. And they tend to be nonischemic in etiology. So, I think that kind of restricts our analysis. And perhaps, I guess, future studies could model using female tissues, for example, instead of only male. But the limitation of all human studies is sample availability. And perhaps, human organoid research can be less limited by that. And certainly, mouse research has become more evenly distributed of male and female mice.   Cindy St. Hilaire:        Yeah. Suffice it to say, human research is hard, but you managed to do an amazing and really important study. It was really elegant and well done. Congratulations on what is an epic amount of time. 12-hour experiments are no joke, and really beautiful data. So, thank you so much for joining me today, Dr Nguyen and Miss almost Dr D'Addabbo. Congrats and I'm really looking forward to seeing your future work.   Jessica D'Addabbo:    Thank you so much.   Patricia Nguyen:         Thanks so much.   Jessica D'Addabbo:    Thank you for having us. This is wonderful.   Cindy St. Hilaire:        That's it for the highlights from the April 29th and May 13th issues of Circulation Research. Thank you so much for listening. Please check out the Circ Res Facebook page and follow us on Twitter and Instagram with the handle @Circres and #Discover CircRes. Thank you to our guests: Dr Patricia Nguyen, and soon to be Doctor, Jessica D'Addabbo, from Stanford University.   This podcast was produced by Ishara Ratnayaka, edited by Melissa Stoner, and supported by the editorial team of Circulation Research. Copy text for the highlighted articles was provided by Ruth Williams. I'm your host, Dr Cindy St. Haler. And this is Discover CircRes, you're on the go source for the most exciting discoveries in basic cardiovascular research. This program is copyright of the American Heart Association 2022. The opinions expressed by the speakers of this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more information, visit aha journals.org.  

This episode is also available as a blog post: https://drdannielleblumenthal.wordpress.com/2022/03/12/validation-of-animal-models-for-viral-hemorrhagic-fever-syndrome-using-acute-human-data/

Tired of the amyloid cascade hypothesis? Think there's more to AD than the plaques and tangles? You've come to the right place! Elyn is back for her final episode covering papers from 2021 on Vascular Contributions to Alzheimer Disease. Tune in to hear about the latest findings relating to cerebrovascular changes in AD, and why they matter.  Sections in this episode:  Insights from Clinical Studies (4:10)  Insights from Animal Models (14:47) -------------------------------------------------------------- To find the numbered bibliography with all the papers covered in this episode, click here, or use the link below:https://drive.google.com/file/d/1S2OmhcNjWt4Fs4kGSHCV93Vp2LRaXZx9/view?usp=sharingTo access the folder with all the bibliographies for 2021 papers, follow this link (it will be updated as we publish episodes and process bibliographies), or click the following link below:https://drive.google.com/drive/folders/1N1zx_itPkCDNYE1yFGZzQxDDR-NiRx3p?usp=sharingYou can also find all of our bibliographies on our website: www.amindr.com. --------------------------------------------------------------Follow-up on social media for more updates!Facebook:  AMiNDR  Twitter: @AMiNDR_podcastInstagram: @AMiNDR.podcastYoutube: AMiNDR PodcastLinkedIn: AMiNDR PodcastEmail: amindrpodcast@gmail.com  -------------------------------------------------------------- Please help us by spreading the word about AMiNDR to your friends, colleagues, and networks! Another way you can help us reach more listeners who would benefit from the show is by rating and/or reviewing us on Apple Podcasts, Spotify, or wherever you listen to podcasts. It helps us a lot and we thank you in advance for leaving a review! Thank you to our sponsor, the Canadian Consortium of Neurodegeneration in Aging, or CCNA, for their financial support of this podcast. This helps us to stay on the air and bring you high quality episodes. You can find out more about the CCNA on their website: https://ccna-ccnv.ca/. Our team of volunteers works tirelessly each month to bring you every episode of AMiNDR. This episode was scripted and hosted by Elyn Rowe, edited by Ellen Koch, and reviewed by Kate Van Pelt and Anusha Kamesh. The bibliography was made by Lara Onbasi and the wordcloud was created by Sarah Louadi (www.wordart.com). Big thanks to the sorting team for taking on the enormous task of sorting all of the Alzheimer's Disease papers into episodes each month. For December 2021, the sorters were Jacques Ferreira, Christy Yu, Kate Van Pelt, Kira Tosefsky, Dana Clausen, Eden Dubchak, Ben Cornish, Ellen Koch, and Elyn Rowe.Also, props to our management team, which includes Sarah Louadi, Ellen Koch, Naila Kuhlmann, Elyn Rowe, Anusha Kamesh, Jacques Ferreira for keeping everything running smoothly.Our music is from "Journey of a Neurotransmitter" by musician and fellow neuroscientist Anusha Kamesh; you can find the original piece and her other music on soundcloud under Anusha Kamesh or on her YouTube channel, AKMusic.   https://www.youtube.com/channel/UCMH7chrAdtCUZuGia16FR4w   -------------------------------------------------------------- If you are interested in joining the team, send us your CV by email. We are specifically looking for help with sorting abstracts by topic, abstract summaries and hosting, audio editing, creating bibliographies, and outreach/marketing. However, if you are interested in helping in other ways, don't hesitate to apply anyways.  --------------------------------------------------------------*About AMiNDR: *  Learn more about this project and the team behind it by listening to our first episode: "Welcome to AMiNDR!" 

Interested in a fresh perspective on the etiology of AD? Join Elyn for her monthly tour through the new research on vascular contributions to Alzheimer disease! Whether this is your niche field, or you want to look at the disease through a new lens, this episode is perfect for you. Tune in to hear about endothelial cell biology, a phase 2 clinical trial, and several animal models!  Sections in this episode:  Endothelial Cell Biology & Amyloid Clearance (4:40)  Insights from Animal Models (8:44)  Insights from Human Studies (13:49) -------------------------------------------------------------- To find the numbered bibliography with all the papers covered in this episode, click here, or use the link below:https://drive.google.com/file/d/1QGGPowwqeKdcBm7MHLofpRxy2FfpqpdQ/view?usp=sharingTo access the folder with all the bibliographies for 2021 papers, follow this link (it will be updated as we publish episodes and process bibliographies), or click the following link below:https://drive.google.com/drive/folders/1N1zx_itPkCDNYE1yFGZzQxDDR-NiRx3p?usp=sharingYou can also find all of our bibliographies on our website: www.amindr.com. --------------------------------------------------------------Follow-up on social media for more updates!Facebook:  AMiNDR  Twitter: @AMiNDR_podcastInstagram: @AMiNDR.podcastYoutube: AMiNDR PodcastLinkedIn: AMiNDR PodcastEmail: amindrpodcast@gmail.com  -------------------------------------------------------------- Please help us by spreading the word about AMiNDR to your friends, colleagues, and networks! Another way you can help us reach more listeners who would benefit from the show is by rating and/or reviewing us on Apple Podcasts, Spotify,  or wherever you listen to podcasts. It helps us a lot and we thank you in advance for leaving a review! Our team of volunteers works tirelessly each month to bring you every episode of AMiNDR. This episode was scripted and hosted by Elyn Rowe, edited by Michelle Grover, and reviewed by Jacques Ferreira and Anusha Kamesh.  The bibliography was made by Lara Onbasi, and the wordcloud was created by Sarah Louadi (www.wordart.com). Big thanks to the sorting team for taking on the enormous task of sorting all of the Alzheimer's Disease papers into episodes each month. For November 2021, the sorters were Jacques Ferreira, Christy Yu, Kate Van Pelt, Kira Tosefsky, Dana Clausen, Nicole Corso, Eden Dubchak, Ben Cornish, Ellen Koch, Elyn Rowe, and Naila KuhlmannAlso, props to our management team, which includes Sarah Louadi, Ellen Koch, Naila Kuhlmann, Elyn Rowe, Anusha Kamesh, Jacques Ferreira for keeping everything running smoothly.Our music is from "Journey of a Neurotransmitter" by musician and fellow neuroscientist Anusha Kamesh; you can find the original piece and her other music on soundcloud under Anusha Kamesh or on her YouTube channel, AKMusic.   https://www.youtube.com/channel/UCMH7chrAdtCUZuGia16FR4w   -------------------------------------------------------------- If you are interested in joining the team, send us your CV by email. We are specifically looking for help with sorting abstracts by topic, abstract summaries and hosting, audio editing, creating bibliographies, and outreach/marketing. However, if you are interested in helping in other ways, don't hesitate to apply anyways.  --------------------------------------------------------------*About AMiNDR: *  Learn more about this project and the team behind it by listening to our first episode: "Welcome to AMiNDR!" 

PharmaDrug Inc CEO Daniel Cohen tells Proactive the group announced a positive research result for its preclinical cancer study which evaluated the effectiveness of cepharanthine-2HCI alone or when used in combination with standard of care (SoC) chemotherapy on four undisclosed cancer types. The company said that it is now focusing on advancing Investigational New Drug enabling studies to support future FDA clinical studies in 2022 for cepharanthine. Cohen says moving research from in vitro (cell culture-based models) into accepted animal models of cancer is a critical step along its path to the clinic.

Dr Kamar Ameen-Ali narrates her blog written for NIHR Dementia Researcher. Why have preclinical studies using Alzheimer's disease mouse models failed to translate into successful clinical trials? Kamar explores the topic, and how the system could be improved. Find the original text, and narration here on our website. https://www.dementiaresearcher.nihr.ac.uk/has-a-reliance-on-animal-models-delayed-progress-in-dementia-research/ If you would like to write your own blog drop us a line, we're always on the look out for new contributors to write about their research, careers + more dementiaresearcher@nihr.ac.uk 

Curious about how neuronal hyperactivity and hippocampal synaptic plasticity impairment contribute to Alzheimer's pathology? Join Glory for the latest updates on research about the mechanisms of synaptic transmission and plasticity affected in Alzheimer's disease. This month, June 2021, delivers 17 new papers that will fill you in on all things synaptic in AD! Give it a listen to find out more and stimulate your own synapses!   Sections in this episode:  Synapse Function and Plasticity (2:17)  Neurotransmitter Systems Affected in AD (11:04)  Neuronal Hyperactivity and Calcium Signaling (18:45)  Spatial Memory (24:30)  Animal Models (29:30)  -------------------------------------------------------------- You can find the numbered bibliography for this episode by clicking here, or the link below:https://drive.google.com/file/d/1d3Zk1ez98ExtQ6_A0lGSbsMR6xmcVvDT/view?usp=sharingTo access the folder with all the bibliographies for 2021 so far, follow this link (it will be updated as we publish episodes and process bibliographies), or click the following link below:https://drive.google.com/drive/folders/1N1zx_itPkCDNYE1yFGZzQxDDR-NiRx3p?usp=sharingYou can also join our mailing list to receive a newsletter by filling this form. Or tweet at us: @AMiNDR_podcast  --------------------------------------------------------------Follow-up on social media for more updates!Facebook:  AMiNDR  Twitter: @AMiNDR_podcastInstagram: @AMiNDR.podcastYoutube: AMiNDR PodcastLinkedIn: AMiNDR PodcastIf you have any questions or concerns, do not hesitate to contact us at: amindrpodcast@gmail.com  -------------------------------------------------------------- Please help us by spreading the word about AMiNDR to your friends, colleagues, and networks! Another way you can help us reach more researchers is by leaving us a review on Apple Podcasts or wherever you listen to podcasts. We would like to thank our amazing team for all of the work that goes into every episode of AMiNDR. Today's episode was scripted and hosted by Glory Nasseri, edited by Chihiro Abe, and reviewed by Anusha Kamesh. The bibliography was created by Jacques Ferreira and wordcloud (wordart.com) generated by Sarah Louadi. Big thanks to the sorting team for sorting all the papers published in June into themes for our episodes: Jacques Ferreira, Elyn Rowe, Ellen Koch, Christy Yu, Nicole Corso, Sarah Louadi, and Naila Kuhlmann. Also, props to our management team, which includes Sarah Louadi, Ellen Koch, Naila Kuhlmann, Elyn Rowe, Anusha Kamesh, and Jacques Ferreira, for keeping everything running smoothly.Our music is from "Journey of a Neurotransmitter" by musician and fellow neuroscientist Anusha Kamesh; you can find the original piece and her other music on soundcloud under Anusha Kamesh or on her YouTube channel, AKMusic.   https://www.youtube.com/channel/UCMH7chrAdtCUZuGia16FR4w   -------------------------------------------------------------- If you are interested in joining the team, send us your CV by email. We are specifically looking for help with sorting abstracts by topic, abstract summaries and hosting, creating bibliographies, and promotions. However, if you are interested in helping in other ways, don't hesitate to apply anyways.  --------------------------------------------------------------*About AMiNDR: *  Learn more about this project and the team behind it by listening to our first episode: "Welcome to AMiNDR!" 

In this episode, we chat with Aubrey de Grey about Aging, Longevity, and Animal Models. Ever wondered why opossums live 1.5x as long on a remote island on the Outer Banks of Virginia? Why do Tortoises live so long? Why is breathing so bad for us? And what the roadmap for treating aging looks like. 

In this episode, Courtney takes you through the papers from March of 2021 on the Role of Immune systems and glial cells in Alzheimer's disease pathology! We will be discussing papers related to neuroinflammatory pathways in microglia and astrocytes, systemic inflammation and so much more! Tune in for this exciting episode!  Sections in this episode: Systemic Inflammation (2.02) Neuroinflammation in Humans (6.27) Astrocytes in AD (9.41) Microglia in AD (13.24) Neuroinflammation in Animal Models (27.38)  --------------------------------------------------------------You can find the bibliography for this episode by clicking here. To access the folder with all the bibliographies for 2021 so far, follow this link (it will be updated as we publish episodes and process bibliographies), or click the following link below:https://drive.google.com/drive/folders/1N1zx_itPkCDNYE1yFGZzQxDDR-NiRx3p?usp=sharingYou can also join our mailing list to receive a newsletter once per month by filling this form. Or tweet at us: @AMiNDR_podcast  --------------------------------------------------------------We would appreciate your feedback so we can better cater to your needs.  You can fill our feedback form here:    https://forms.gle/5aq2JyrT6g4P1m8v6 You can also share your thoughts and suggestions by contacting us:  Email: amindrpodcast@gmail.com  Facebook:  AMiNDR  Twitter: @AMiNDR_podcastInstagram: @AMiNDR.podcastYoutube: AMiNDR Podcast-------------------------------------------------------------- Please help us by spreading the word about AMiNDR to your friends, colleagues, and networks! Another way you can help us reach more researchers is by leaving us a review on Apple Podcasts. We would like to thank our amazing team for all of the work that goes into every episode of AMiNDR. Today's episode was scripted and hosted by Courtney Kloske, reviewed by Vyshnavy Balendra, and edited by Anusha Kamesh. The bibliography was created by Jacques Ferreira and the wordcloud was generated by Sarah Louadi (www.wordart.com). Big thanks to the sorting team for sorting all the papers published in March into themes for our episodes, and to our management team, which includes Sarah Louadi, Ellen Koch, Naila Kuhlmann, Elyn Rowe, Anusha Kamesh, and Jacques Ferreira, for keeping everything running smoothly.Our music is from "Journey of a Neurotransmitter" by musician and fellow neuroscientist Anusha Kamesh; you can find the original piece and her other music on soundcloud under Anusha Kamesh or on her YouTube channel, AKMusic.   https://www.youtube.com/channel/UCMH7chrAdtCUZuGia16FR4w   -------------------------------------------------------------- If you are interested in joining the team, send us your CV by email. We are specifically looking for help with sorting abstracts by topic, abstract summaries and hosting, creating bibliographies, and promotions. However, if you are interested in helping in other ways, don't hesitate to apply anyways.  --------------------------------------------------------------*About AMiNDR: *  Learn more about this project and the team behind it by listening to our first episode: "Welcome to AMiNDR!"  

Dr. Nicole Avena is a research neuroscientist and a pioneer in the field of food addiction. Her seminal research work jump-started a new field of exploration in medicine and nutrition. She is an expert in diet during pregnancy and baby, toddler and childhood nutrition. She has published over 90 scholarly journal articles, as well as several book chapters and books, on topics related to food, addiction, obesity and eating disorders. She also edited the books, "Animal Models of Eating Disorders" (2012) and "Hedonic Eating" (2015), coauthored the popular book of food and addiction called "Why Diets Fail" (Ten Speed Press), and recently finished her new book, "What to Eat When You Want to Get Pregnant." Her research achievements have been honored by awards from several groups including the New York Academy of Sciences, the American Psychological Association, the National Institute on Drug Abuse, and her research has been funded by the National Institutes of Health (NIH) and National Eating Disorders Association. She also maintains a blog, Food Junkie, with Psychology Today. Follow Nicole: Order Her Books: http://www.drnicoleavena.com Watch her TED -Ed: https://ed.ted.com/lessons/how-sugar-affects-the-brain-nicole-avena Twitter: @DrNicoleAvena   The content of our show is educational only. It does not supplement or supersede the professional relationship and direction of your healthcare provider. Always seek the advice of your physician or other qualified mental health providers with any questions you may have regarding a medical condition, substance use disorder, or mental health concern.

Welcome back to Neurotech Pub!In this episode, host and Paradromics CEO, Matt Angle, speaks with Beata Jarosiewicz, Vikash Gilja, Sergey Stavisky, and Frank Willett about how brain computer interfaces can be used to restore communication in patients with tetraplegia. They take a deep dive into state of the art thought-to-text technology compared with the current state of speech decoding.Check out full video with transcript here: https://www.paradromics.com/podcast/neurotech-pub-episode-2-what-weve-got-here-is-failure-to-communicate 1:49 Braingate Clinical Trial Program |2:32 Beata's New Job at Neuralink |2:43 Stanford Neural Prosthetics Translational Laboratory |2:53 Leigh Hochberg |3:05 Andy Schwartz |5:14 2020 BCI Award|8:44 Subjective Experience of Control |10:39 Closed Loop Calibration |12:08 Animal Models for Prosthesis Development |14:21 Keyboard Optimization |15:33 Tablet PC Control Papers | See Also |16:01 Palm Pilot Graffiti |16:24 Frank's Preprint on Handwriting |17:40 Video Abstract on Frank's Work |21:38 Penfield and Boldrey 1937 |22:04 A Quick, Lay Summary of Penfield's Work |24:21 Hand Knob |26:43 Output-Null Neural State Space Dimensions |34:23 Matt Kaufman's Work |38:29 Vikash's work with Paul Nuyujukian |39:07 Mark Churchland |42:01 Review Paper by Eb Fetz |44:18 Chang Lab at UCSF |44:46 Robert Knight's Group on Speech Decoding | Imagined Speech |50:38 Speech Decoding in Hand Knob |50:55 Phoneme Decoding |52:48 Auditory Decoding in NHPs |54:58 Moses et al., 2019|55:12 Makin et al., 2020 |1:07:11 Nir's Paper on Error Signals |Want more? Follow Paradromics & Neurotech Pub on Twitter  Follow Matt A and Sergey Stavisky on Twitter

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.11.16.385286v1?rss=1 Authors: Montes-Lourido, P., Kar, M., Kumbam, I., Sadagopan, S. Abstract: Estimates of detection and discrimination thresholds are often used to explore broad perceptual similarities between human subjects and animal models. Pupillometry shows great promise as a non-invasive, easily-deployable method of comparing human and animal thresholds. Using pupillometry, previous studies in animal models have obtained threshold estimates to simple stimuli such as pure tones, but have not explored whether similar pupil responses can be evoked by complex stimuli, what other stimulus contingencies might affect stimulus-evoked pupil responses, and if pupil responses can be modulated by experience or short-term training. In this study, we used an auditory oddball paradigm to estimate detection and discrimination thresholds across a wide range of stimuli in guinea pigs. We demonstrate that pupillometry yields reliable detection and discrimination thresholds across a range of simple (tones) and complex (conspecific vocalizations) stimuli; that pupil responses can be robustly evoked using different stimulus contingencies (low-level acoustic changes, or higher level categorical changes); and that pupil responses are modulated by short-term training. These results lay the foundation for using pupillometry as a high-throughput method of estimating thresholds in large experimental cohorts, and unveil the full potential of using pupillometry to explore broad similarities between humans and animal models. Copy rights belong to original authors. Visit the link for more info

Having trouble keeping up with the literature in Alzheimer's Disease? We are here to help!In this episode, Marcia covers papers published in June 2020 on treatment development done on animal models, targeting metabolism, mitochondria, oxidative stress, the gut microbiome, inflammatory pathways, glia, and autophagy. If you are interested in learning more about these pathological events, you should check out our episode on these disease mechanisms, covered by Anusha. We also have a number of episodes dedicated to pre-clinical testing, split by the intended target the cholinergic system, the glutamatergic system, synaptic function, tau, amyloid-beta, cognitive performance, and other multitargeted approaches.  Enjoy! To receive the list of papers covered (with timestamps), please fill this form: -------->  https://forms.gle/CVVbznAFM8pamdgk6  -------or by tweeting at us: @AMiNDR_podcast-----------------------------------------------------------------------List of sections in this episode: (0.57)   Metabolism / lipids(3.40)   The gut microbiome(5.00)   Autophagy(8.10)     Mitochondria(10.54)   Oxidative stress(18.25)   Inflammatory pathways/ glia-----------------------------------------------------------------------We would appreciate your feedback so we can better cater to your needs.  You can fill our feedback form here ---------->  https://forms.gle/5aq2JyrT6g4P1m8v6You can also share your thoughts and suggestions by contacting us: Email: amindrpodcast@gmail.comFacebook:  AMiNDRTwitter: @AMiNDR_podcast*New* Instagram: @AMiNDR.podcast-----------------------------------------------------------------------Today's episode was scripted and hosted by Marcia Jude, edited by Anusha Kamesh, and made possible by an entire team of volunteers behind the scenes.  Our music is from "Journey of a Neurotransmitter" by musician and fellow neuroscientist Anusha Kamesh; you can find the original piece and her other music on soundcloud under Anusha Kamesh or on her YouTube channel, AKMusic https://www.youtube.com/channel/UCMH7chrAdtCUZuGia16FR4w -----------------------------------------------------------------------If you are interested in joining the team, send us your CV by email. We are specifically looking for help with abstract summary and podcast editing. However, if you are interested in helping in other ways, don't hesitate to apply anyways. -----------------------------------------------------------------------*About AMiNDR: *Learn more about this project and the team behind it by listening to our first episode: "Welcome to AMiNDR!"

Having trouble keeping up with the literature in Alzheimer's Disease? We are here to help!In this episode, Naila covers papers published in June 2020 on treatment development done on animal models, targeting the cholinergic system, the glutamatergic system, synaptic function, tau, and amyloid-beta. If you are interested in this topic, you should check out our other episodes on this topic from the same month, where the approach targeted oxidative stress, inflammation, autophagy, cognitive function...Enjoy! To receive the list of papers covered (with timestamps), please fill this form: -------->  https://forms.gle/CVVbznAFM8pamdgk6  -------or by tweeting at us: @AMiNDR_podcast-----------------------------------------------------------------------List of sections in this episode: (2:21)            Acetylcholinesterase/the cholinergic system       (6:35)          The glutamatergic system(10:25)         Synaptic function(20:23)         Tau phosphorylation/tau protein(24:07)         Amyloid-beta mediated toxicity & production(35:25)         Other-----------------------------------------------------------------------We would appreciate your feedback so we can better cater to your needs.  You can fill our feedback form here ---------->  https://forms.gle/5aq2JyrT6g4P1m8v6You can also share your thoughts and suggestions by contacting us: Email: amindrpodcast@gmail.comFacebook:  AMiNDRTwitter: @AMiNDR_podcast*New* Instagram: @AMiNDR.podcast-----------------------------------------------------------------------Today's episode was scripted and hosted by Naila Kuhlmann, edited by Anusha Kamesh, and made possible by an entire team of volunteers behind the scenes.  Our music is from "Journey of a Neurotransmitter" by musician and fellow neuroscientist Anusha Kamesh; you can find the original piece and her other music on soundcloud under Anusha Kamesh or on her YouTube channel, AKMusic https://www.youtube.com/channel/UCMH7chrAdtCUZuGia16FR4w -----------------------------------------------------------------------If you are interested in joining the team, send us your CV by email. We are specifically looking for help with abstract summary and podcast editing. However, if you are interested in helping in other ways, don't hesitate to apply anyways. -----------------------------------------------------------------------*About AMiNDR: *Learn more about this project and the team behind it by listening to our first episode: "Welcome to AMiNDR!"

About the bibliography: To receive the list of papers covered (with time-stamps), please subscribe to our mailing list. You can do so by filling this form:   https://forms.gle/jJM9dK4SufapQkey8 or by sending us an email at amindrpodcast@gmail.com List of sections in this episode: Lab techniques (1.35)New animal models (19.32)Old animal models (27.16)New cellular models (28.27)Tissue engineering (32.42)Human methodology (34.14)Computational modeling (47.48) This episode was curated and produced by a group of volunteers. As we work on producing full-length episodes on ALL the publications from June 2020, we would appreciate your feedback so we can better cater to your needs. You can fill our feedback form here: https://forms.gle/5aq2JyrT6g4P1m8v6  You can also share your thoughts and suggestions by contacting us: Email: amindrpodcast@gmail.comTwitter: @AMiNDR_podcast If you are interested in joining the team, send us your CV by email. We are specifically looking for help with abstract summary and podcast editing. However, if you are interested in helping in other ways, don't hesitate to apply anyways.  *About AMiNDR: *Learn more about this project and the team behind it by listening to our first episode: "Welcome to AMiNDR!" Our next trial episodes for the month of February 2020: Genetics, Risk Factors & New diagnostic tools, Treatments and Testing, Miscellaneous.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.05.05.078618v1?rss=1 Authors: De Lorenzo, F., Luningschror, P., Nam, J., Pilotto, F., Galli, E., Lindholm, P., Rudt von Collenberg, C., Tii Mungwa, S., Kauder, J., Jablonka, S., Petri, S., Lindholm, D., Saxena, S., Sendtner, M., Saarma, M., Voutilainen, M. H. Abstract: Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease primarily afflicting motor neurons (MNs) of the spinal cord, brainstem, and motor cortex, leading to paralysis and eventually death within 3 to 5 years of diagnosis. No cure or effective therapy to halt ALS progression is available. The role of chronic endoplasmic reticulum (ER) stress in the pathophysiology of ALS, as well as a potential drug target, has received increasing attention. Here, we investigated the therapeutic effect of the ER resident protein cerebral dopamine neurotrophic factor (CDNF) in preclinical models of ALS harboring different genetic mutations. We identify that intracerebroventricular (i.c.v.) administration of CDNF significantly halts the progression of the disease and improves motor behavior in TDP43-M337V and SOD1-G93A rodent models of ALS. CDNF rescues MNs in vitro and in vivo from ER stress associated cell death and its beneficial effect is independent of genetic disease etiology. Notably, CDNF regulates the unfolded protein response (UPR) initiated by transducers IRE1, PERK, and ATF6, thereby enhancing MN survival. Thus, CDNF holds great promise for the design of new rational treatments for ALS. Copy rights belong to original authors. Visit the link for more info

Insights from Animal Models of Obesity and Asthma

------------------Support the channel------------ Patreon: https://www.patreon.com/thedissenter SubscribeStar: https://www.subscribestar.com/the-dissenter PayPal: paypal.me/thedissenter PayPal Subscription 1 Dollar: https://tinyurl.com/yb3acuuy PayPal Subscription 3 Dollars: https://tinyurl.com/ybn6bg9l PayPal Subscription 5 Dollars: https://tinyurl.com/ycmr9gpz PayPal Subscription 10 Dollars: https://tinyurl.com/y9r3fc9m PayPal Subscription 20 Dollars: https://tinyurl.com/y95uvkao ------------------Follow me on--------------------- Facebook: https://www.facebook.com/thedissenteryt/ Twitter: https://twitter.com/TheDissenterYT Anchor (podcast): https://anchor.fm/thedissenter Dr. Jonathon Crystal is Professor of Psychological and Brain Sciences at Indiana University. His research focuses on developing animal models of cognition. His current work focuses on episodic memory, source memory, and prospective memory in rats. He has also developed rodent models to assess retrieval practice, working memory, and metacognition. He is currently the Editor of Learning & Behavior, and he recently served as President of the Comparative Cognition Society. In this episode, we talk about studying memory in nonhuman animals, primarily in rats. First, we talk about ways of classifying different types of memory. We then get into how Dr. Crystal designs experiments to study different types of memory and know if they even exist in other animals, including episodic memory and prospective memory. Toward the end, we also refer to metacognition. -- Follow Dr. Crystal's work: Faculty page: https://bit.ly/2VxsVft Articles on Researchgate: https://bit.ly/2JOjK8v Relevant papers: Animal Models of Episodic Memory: https://bit.ly/2RIIHEl Episodic-like Memory in the Rat: https://bit.ly/2ZK1ZM5 Prospective memory in the rat: https://bit.ly/2X1JSjd Metacognition in animals: https://bit.ly/31TqxnN -- A HUGE THANK YOU TO MY PATRONS: KARIN LIETZCKE, ANN BLANCHETTE, SCIMED, PER HELGE HAAKSTD LARSEN, LAU GUERREIRO, RUI BELEZA, MIGUEL ESTRADA, ANTÓNIO CUNHA, CHANTEL GELINAS, JERRY MULLER, FRANCIS FORD, HANS FREDRIK SUNDE, BRIAN RIVERA, ADRIANO ANDRADE, YEVHEN BODRENKO, SERGIU CODREANU, ADAM BJERRE, ŁUKASZ STAFINIAK, AIRES ALMEIDA, BERNARDO SEIXAS, HERBERT GINTIS, RUTGER VOS, AND RICARDO VLADIMIRO! A SPECIAL THANKS TO MY PRODUCERS, YZAR WEHBE, ROSEY, AND JIM FRANK!

Sal, Adam & Justin interview Dr. Nicole Avena about the affect of sugar and sugar substitutes in the diet and how they affect the brain. This is a must listen if you have a sweet tooth. You can also catch Dr. Avena's TED presentation here: http://ed.ted.com/lessons/how-sugar-affects-the-brain-nicole-avena You can find Dr. Avena at www.drnicoleavena.com Dr. Avena is a research neuroscientist, author and expert in the fields of nutrition, diet and addiction. She received a Ph.D. in Neuroscience and Psychology from Princeton University, followed by a postdoctoral fellowship in molecular biology at The Rockefeller University in New York City. She has published over 70 scholarly journal articles, as well as several book chapters and books, on topics related to food, addiction, obesity and eating disorders. She also edited the books, "Animal Models of Eating Disorders" (2012) and "Hedonic Eating" (2015), coauthored the popular book of food and addiction called "Why Diets Fail" (Ten Speed Press), and recently finished her new book, "What to Eat When You're Pregnant." Her research achievements have been honored by awards from several groups including the New York Academy of Sciences, the American Psychological Association, the National Institute on Drug Abuse, and her research has been funded by the National Institutes of Health (NIH) and National Eating Disorders Association. She also maintains a blog, Food Junkie, with Psychology Today. Get our newest program, Kettlebells 4 Aesthetics (KB4A), which provides full expert workout programming to sculpt and shape your body using kettlebells. Only $7 at www.mindpumpmedia.com! Get MAPS Prime, MAPS Anywhere, MAPS Anabolic, MAPS Performance, MAPS Aesthetic, the Butt Builder Blueprint, the Sexy Athlete Mod AND KB4A (The MAPS Super Bundle) packaged together at a substantial DISCOUNT at www.mindpumpmedia.com. Make EVERY workout better with MAPS Prime, the only pre-workout you need… it is now available at mindpumpmedia.com Have Sal, Adam & Justin personally train you via video instruction on our YouTube channel, Mind Pump TV. Be sure to Subscribe for updates. Get your Kimera Koffee at www.kimerakoffee.com, code "mindpump" for 10% off! Got a beard? Condition your beard with Big Top Beard Company's natural oils and organic essential oil blends to make it not only feel great but smell amazing! Get Big Top Beard Company products at www.bigtopbeardcompany.com, code "mindpump" for 33% off. Add to the incredible brain enhancing effect of Kimera Koffee with www.brain.fm/mindpump 10 Free sessions! Music for the brain for incredible focus, sleep and naps! Please subscribe, rate and review this show! Each week our favorite reviewers are announced on the show and sent Mind Pump T-shirts!

David Rosenblum discusses ABA Pain Syllabus topic- Animal Models of Pain and Ethics of Animal Experimentation Common animal models in the study of pain Ethics of animal experimentation Other-General: Animal models of pain and ethics of animal experimentation Also be sure to check out next weeks webinar_

Guest Rogue: Dr. Ray Greek - The Science of Animal Models; This Day in Skepticism; News Items: Homeopathy Pseudoscience, Teachers Cautious about Evolution; Who's That Noisy; Your Questions and E-mails: Countering Fallacies; Name That Logical Fallacy; Science or Fiction

Guest: Richard Karas, MD, PhD Host: Michael Benson, MD What do our animal friends have to tell us about the effects of hormones on cardiovascular risk? Does a mouse or monkey really have anything to teach us? Our guest today is Dr. Richard Karas, Professor of Medicine, at the Tufts University School of Medicine in Boston. He has several titles including: Co-Director, Molecular Cardiology Research Center, Director, Preventive Cardiology and Director, Women's Heart Center at the New England Medical Center. He received his MD from Tufts and his Ph.D in Physiology from Harvard.

Enhanced Video PodcastAired date: 2/21/2007 3:00:00 PM Eastern Time

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