Podcasts about Tau protein

Broadcast from KSQD, Santa Cruz on 4-03-2025: Dr. Dawn provides a comprehensive explanation of vertigo versus dizziness, describing inner ear anatomy, how displaced crystals cause positional vertigo, and various treatment maneuvers including the Epley, Sarmont, and Foster techniques. Responding to an email from a listener suffering from both vertigo and tinnitus, she recommends exploring chiropractic adjustment for the tinnitus and special electroacupuncture treatments while suggesting additional vestibular testing might be beneficial. Dr. Dawn addresses an email about POTS (Postural Orthostatic Tachycardia Syndrome) likely caused by long COVID, recommending diagnostic tests, mitochondrial support supplements, low-dose naltrexone, and investigating possible heavy metal release due to significant weight loss. A caller with Dupuytren's contracture describes frustrations with Medicare Advantage limitations and surgical options, with Dr. Dawn discussing quality of life impacts, the differences between open and minimally invasive procedures, and possible workarounds including voice-to-text technology. The show concludes with Dr. Dawn discussing how a falsified 2006 research paper led Alzheimer's research astray for decades by incorrectly focusing on amyloid beta protein removal, resulting in questionable drug approvals despite expert objections, while better evidence points to tau protein as a more reliable disease marker.

Guest Michael Greicius is an authority on Alzheimer's disease. He makes the case that while effective treatments have remained elusive, there are high hopes for new approaches that target tau proteins in the brain associated with the disease. In the meantime, to reduce Alzheimer's risk stay active, eat well, and manage circulatory risks, but skip genetic testing for now until better treatments emerge, Greicius tells host Russ Altman on this episode of Stanford Engineering's The Future of Everything podcast.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:  Michael GreiciusConnect 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) IntroductionRuss Altman introduces guest Michael Greicius, a professor of neurology and neurological sciences at Stanford University.(00:02:12) Understanding Alzheimer's DiseaseThe roles of amyloid and tau proteins in Alzheimer's disease.(00:04:53) Challenges in Developing TreatmentsThe multiple hurdles in creating Alzheimer's therapies.(00:09:07) Current Alzheimer's DrugsThe controversies and limitations of recently approved drugs.(00:10:23) Amyloid Plaques and Their ImpactWhy removing amyloid plaques hasn't improved patient outcomes.(00:14:29) Problems with Alzheimer's TrialsThe disconnect between amyloid removal and patient outcomes.(00:18:03) Functional Unblinding and Trial BiasHow functional unblinding affects trial results and drug evaluations.(00:23:51) The Potential of Targeting TauNew breakthroughs in targeting tau protein for Alzheimer's.(00:26:35) The Future of PreventionPotential preemptive treatments for Alzheimer's and their administration.(00:29:19) Lifestyle and Risk ReductionRecommendations for reducing risk of Alzheimer's disease.(00:31:43) 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

CTE is surprisingly common - but, it can only be diagnosed post-mortem, and by a forensic expert. So, how is does an examination work? And why is it so hard to have one done?  Dr Linda Iles is a forensic neuropathologist, and someone who performs post-mortem brain examinations on people every single day. What she discovers in these exams is extraordinary, and revealing of the life that person lead.  Understand how someone is diagnosed with CTE post-mortem, and the intricate details of brain examinations with host Kathryn Fox; as she chats with Victorian Institute of Forensic Medicine's Dr Linda Iles.  Crime Insiders executive producer Dan Mullins presents a look back at one of our earlier episodes. For more information on CTE or if anyone you know is showing symptoms and you need support, visit the following resources:  https://www.concussionfoundation.com.au/helplineSee omnystudio.com/listener for privacy information.

Broadcast from KSQD Santa Cruz on 6-13-2024 Alzheimer's Disease and APOE4 Gene Listener asks about the APOE4 gene and its association with Alzheimer's disease in the light of a recent sensationalistic Nature publication. The impact of amyloid beta and TAU proteins on Alzheimer's pathology. Differences in Alzheimer's risk among different ethnic groups with APOE4 with emphasis on the importance of cholesterol levels as a risk multiplier. Advice for a listener's husband dealing with chronic back pain and sciatica Dr. Dawn presents a basic checklist for evaluating back pain symptoms and determining the need for urgent medical intervention. Potential causes are discussed such as spinal nerve compression from various sources. In this case, Dr. Dawn made a specific suggestion of McKenzie exercises and emphasized the importance of seeing a sports medicine doctor or physiatrist for a comprehensive evaluation. Dr. Dawn responds to a caller about managing knee osteoarthritis The role of glucosamine, chondroitin, and topical diclofenac in treatment. Discussion on non-pharmaceutical approaches like heat application and massage. Potential interventions like steroid injections, hyaluronic acid, platelet rich plasma and their benefits and risks. Dr. Dawn answers a question about dietary oxalates and their impact on kidney stones She emphasizes the importance of the oxalate content in foods and its limited role in kidney stone formation. She emphasizes the importance of hydration and maintaining a healthy microbiome. For specific dietary guidelines on oxalate in foods she suggests using oxalate.org. A concerned parent asks about aluminum and other vaccine adjuvants like formaldehyde for their infant's 2 month well child visit She expresses conflicting fears of being mischaracterized as a vaccine denier by merely expressing concern about vaccination for her infant. Dr. Dawn provides a breakdown of the necessity, immediate urgency and risks of each recommended vaccine (Hepatitis B, DTaP, Polio, Hib, Pneumococcal, Rotavirus) and suggests a social contextualization strategy to perhaps delay Polio, rotavirus and Hep B in this family's social context while emphasizing the importance of certain vaccinations to prevent serious illnesses. Dr. Dawn cites intriguing ambiguities in the literature that support the counterintuitive idea that smaller doses of aluminum may have a greater accumulation in tissues of brain and reproductive tissues than larger doses, and promises to research this further in a future program.

Silver Streakers Fitness & The Role of Tau Protein in Brain Health Grandpa Bill continues revisiting the topic of Alzheimer's, specifically focusing on the fascinating world of Tau protein. Remember that sticky culprit potentially damaging our brain cells? We'll be diving deeper to understand its role in this disease. Here's where you come in, friends! Question 1: Do you have a favorite exercise routine that keeps you feeling young and spry? Share your tips with fellow Silver Streakers! Question 2: Have you or someone you know been impacted by Alzheimer's? What questions do you have about Tau protein and brain health? Join the conversation! Leave a voicemail message with your thoughts and experiences at The BH Sales Kennel Kelp Podcast Message Board. Let's explore healthy living and brain wellness together! #SilverStreakersWorkout, #TauTalk, #BHSKKHHHealingHour,#HealthForAllAges, #AskGrandpaBill, --- Send in a voice message: https://podcasters.spotify.com/pod/show/bhsales/message

Grandpa Bill here, back for another episode on keeping our bodies and minds in tip-top shape. Today, we're taking a deep dive into a fascinating topic: Tau Protein and Dementia. As some of you know, I've had a colorful life. From near-death experiences and auto accidents to the thrills of sports and the challenges of daily life, my head's been through a lot. Now, with all these factors combined, including potential exposure to toxins and the occasional glass of something stronger (wink wink), I can't help but wonder: Could my past be setting the stage for future dementia? Here's where you come in, my friends! Question 1: Have you experienced head trauma or been exposed to industrial toxins? How are you taking care of your brain health proactively? Question 2: Do you have any personal experiences with Tau Protein or dementia? What questions do you have for me? Join the conversation! Share your thoughts and experiences by leaving a voicemail message at The BH Sales Kennel Kelp Holistic Healing Hour Podcast Message Board. Let's learn from each other and explore the exciting world of brain health together! #TauTalk, #DementiaPrevention, #GrandpaBillsStory, #BHSKKHHHealingHour, #AskGrandpaBill. Holistic Health Secrets and Life-Sales Strategies with Grandpa Bill Nourish Your Soul, Boost Your Business: The BH Sales Kennel Kelp Holistic Healing Hour Experience Website: https://www.7kmetals.com/grandpabill Website:https://www.myctfo.com/index.html YouTube: Bill Holt@billholt8792 Social Media: https://www.facebook.com/bill.sales.524 Social Media:https://www.instagram.com/bradybrodyboy12/ Voicemail Message Board: https://podcasters.spotify.com/pod/show/bhsales BH Sales Kennel Kelp Holistic Healing Hour Retired holistic health enthusiast, Grandpa Bill, shares his wisdom and experiences in the realms of health, wealth, and well-being. Join Grandpa Bill on his journey of holistic health and personal growth. With over 45 years of experience in the industry, he has a wealth of knowledge to share on topics ranging from nutrition and supplements, to meditation and spirituality. In his retirement, Grandpa Bill is dedicated to sharing his insights and helping others to achieve their full potential. He is an intuitive thinker, humorist, star seed, poetry fan, with a passion for history and coins. Hosted by Grandpa Bill, 45 year career now retired Disclaimer:This podcast site content is provided for informational purposes only, and does not intend to substitute professional medical advice, diagnosis, or treatment. JOIN US EVERY TUESDAY AT 6PM. EST. https://freedomsnap.org/Seth/ BH Sales Kennel Kelp Holistic Virtual Mall Patriot Supply Link:  ⁠⁠https://mypatriotsupply.com/?rfsn=5615494.137cb6⁠⁠ Health Ranger Link: ⁠⁠https://www.healthrangerstore.com/?⁠⁠rfsn=301296.96452b2&utm_source=HR_Affiliate&utm_campaign=14708&utm_affiliate=301296⁠⁠ ⁠⁠⁠Healer.com⁠⁠⁠: ⁠⁠⁠⁠https://www.HealerCBD.com/?ref=11⁠ https://www.healthrangerstore.com/?rfsn=301296.96452b2&utm_source=HR_Affiliate&utm_campaign=14708&utm_affiliate=301296 --- Send in a voice message: https://podcasters.spotify.com/pod/show/bhsales/message

Um zu wissen, wo man angreifen kann, muss man zunächst wissen, was überhaupt im Gehirn passiert, was die Auslöser der Krankheit sind. Genau damit beschäftigt sich die Biophysikerin Susanne Wegmann seit 17 Jahren. Die Forschungsgruppenleiterin am DZNE-Standort Berlin untersucht das sogenannte Tau-Protein. Dieser körpereigene Eiweißstoff ist für Alzheimer und über 20 neurogenerative Erkrankungen von Bedeutung. Im Gespräch mit Sabine Heinrich erklärt Wegmann, welche Funktion das Tau-Protein im gesunden Gehirn hat, welche Rolle es im erkrankten Gehirn spielt - und dass es dabei noch viele offene Fragen gibt. Doch sie ist zuversichtlich, dass die Rätsel um Tau irgendwann gelöst werden. Im Podcast berichtet Susanne Wegmann, wie eine Anti-Tau-Therapie bei Alzheimer aussehen könnte. Zudem spricht sie mit Sabine Heinrich über ihr Engagement für junge Wissenschaftlerinnen und Wissenschaftler in Mittel- und Südamerika.

Diese Folge findest du auch im Videoformat beim Hauptsponsor der Show ⁠hier⁠. ⁠Hier⁠ findest du im übrigen die aktuell umfangreichste DNA Analyse und Auswertung Deutschlands myGenes von EpiGenes. Du bist total begeistert von der Themenwelt der Epigenetik und möchtest Epigenetic Coach werden? ⁠Hier⁠ findest du alle Informationen dazu. Nach ihrem Studium in Volkswirtschaft hat Kyra Kauffmann ihre ersten beruflichen Schritte im Bankwesen gemacht, im Alter von 29 Jahren folgte die erste Führungsposition, drei Jahre später ist sie dann am chronischen Erschöpfungssyndrom erkrankt. Von dort an hat sie es sich dann zur Aufgabe gemacht die Ursachen ihrer Erkrankung selbst zu erforschen, woraufhin sie auf die modernen naturheilkundlichen Verfahren gestoßen ist.  Inspiriert von deinen eigenen Forschungen hat sie dann die Ausbildung zur Heilpraktikerin gemacht, woraufhin sie sich in ihrer Praxis 2004 selbständig gemacht und sich auf chronische Krankheitsbilder fokussiert hast.  Zudem hast sie heute einen eigenen Podcast, sie gibst Seminare und ist Autorin mehrerer Bücher. Im Interview geht Kyra insbesondere auf genetische Varianten zum APOE Gentyp, auf die Gehirngesundheit, auf Alzheimer und therapeutische Erfolge Alzheimer zu heilen.  Inhalt: 3:45 min: Kyras Kontakt zu individuellen Therapieansätzen mit genetischen Varianten 6:15 min: die Wichtigkeit der Epigenetik auf Basis der Genetik 9:00 min: Brustkrebs und Genetik 9:30 min: BRC1, BRC2 und Krebsrisiko von bis zu 80% 12:30 min: APOE4 das Alzheimergen zu 20% in der Bevölkerung  14:40 min: APOE und der Fetttransport 16:50 min: APOE Genotypen und die Evolution 17:30 min: APOE4 und Immunsystem 18:50 min: SNPs haben immer etwas negatives und positives  20:20 min: TAU Protein und ß-Amyloid in APOE4 Genträgern 26:50 min: APOE unabhängiges Alzheimer und Diabetes 3 29:30 min: APOE, Fette und Hormonmängel 35:00 min: APOE4, Lifestyleempfehlungen, Dr. Dale Bredeson und seine Alzheimerforschungen 40:00 min: APOE4 ist gleich Antikokosfett Gen 42:10 min: oxidiertes LDL testen (LDL Subfraktion) 46:00 min: Schlaf und APOE4/Alzheimer   50:05 min: Dr. Dale Bredesons Behandlungskonzept 55:05 min: Heilungsstadien bei Alzheimer 1:00:05 min: BDNF und die Gehirngesundheit 1:02:25 min: Gene testen lassen   Links: Teste deinen APOE Genotyp mit myGenes360 hier https://www.naturheilkundliche-medizin.de/ LDL Subfraktion  Buch: klar im Kopf www.APOE4.info

CTE is suprisingly common - but, it can only be diagnosed post-mortem, & by a forensic expert. So, how is does an examination work? And why is it so hard to have one done?  Dr Linda Iles is a forensic neuropathologist, and someone who performs post-mortem brain examinations on people every single day. What she discovers in these exams is extraordinary, and telling to the life that person lead.  More recently, CTE has been something she's on the look out for.  Chronic Traumatic Encephalopathy is a progressive degenerative brain disease typically found in individuals with a history of repetitive brain trauma, such as athletes involved in contact sports like AFL, NRL, soccer and martial arts.  Understand how someone is diagnosed post-mortem, and the intricate details of brain examinations with host Kathryn Fox; as she chats with Victorian Institute of Forensic Medicine's Dr Linda Iles.  For more information on CTE or if anyone you know is showing symptoms and you need support, visit the following resources:  https://www.concussionfoundation.com.au/helpline  See omnystudio.com/listener for privacy information.

KSQD 7-12-2023: Public health update for Santa Cruz County, California; Follow up on oral hygiene and the use of hydrogen peroxide; Having pets during pregnancy and early infancy reduces food allergies; Having pets during pregnancy and early infancy reduces food allergies; All about menopause and the brain; Weight training, supplements and other advice for a perimenopausal woman with genetic propensity for diabetes; A cerebral spinal fluid leak is an alternative cause for dementia; Controlling high blood pressure can help reduce dementia; Is expensive new Alzheimer's drug Leqembi worth it? There is now a blood test for Tau protein, a better indicator than beta amyloid

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.14.520487v1?rss=1 Authors: Park, G., Xu, K., Chea, L., Kim, K., Safarta, L., Song, K.-H., Wu, J., Park, S., Min, H., Hiramatsu, N., Han, J., Lin, J. H. Abstract: Tauopathies are neurodegenerative diseases caused by pathologic misfolded tau protein aggregation in the nervous system. Population studies implicate EIF2AK3 (eukaryotic translation initiation factor 2 alpha kinase 3), better known as PERK (protein kinase R-like endoplasmic reticulum kinase), as a genetic risk factor in several tauopathies. PERK is a key regulator of intracellular proteostatic mechanisms, Unfolded Protein Response (UPR) and Integrated Stress Response (ISR). Previous studies found that tauopathy-associated PERK variants encoded functional hypomorphs with reduced signaling in vitro. But, it remained unclear how altered PERK activity led to tauopathy. Here, we chemically or genetically modulated PERK signaling in cell culture models of tau aggregation and found that PERK pathway activation prevented tau aggregation while inhibition exacerbated tau aggregation. In primary tauopathy patient brain tissues, we found that reduced PERK signaling correlated with increased tau neuropathology. We found that tauopathy-associated PERK variants targeted the ER luminal domain; and two of these variants damaged hydrogen bond formation. Our studies support that PERK activity protects against tau aggregation and pathology. This may explain why people carrying hypomorphic PERK variants have increased risk for developing tauopathies. Finally, our studies identify small molecule augmentation of PERK signaling as an attractive therapeutic strategy to treat tauopathies by preventing tau pathology. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Click to sign up for our Compensation Negotiation Workshop: https://www.eventbrite.com/e/compensation-negotiation-workshop-tickets-399319343907?utm-campaign=social&utm-content=attendeeshare&utm-medium=discovery&utm-term=listing&utm-source=cp&aff=escb Lexi and Libby sit down with Kimberly Fiock in today's episode. Kimberly studies brain diseases in a lab and is working toward earning her PHD. With a bachelor's degree in neuroscience & psychology, and a masters in pathology, Kimberly shares her passions and recommendations for how to navigate a PHD program. This episode also touches on mental health. Kimberly shares her personal experiences with having OCD and Bipolar, and gives advice for how to cope with mental health in a high stress STEM field. Follow Kimberly on Instagram: https://www.instagram.com/thepathphd/?hl=en More pathology resources that were talked about in this episode: https://people.rit.edu/~gtfsbi/Symp/highschool.htm https://people.rit.edu/~gtfsbi/Symp/Neuroscience.htm https://people.rit.edu/~gtfsbi/Symp/summer.htm#skip Submit your review to the google form here to be entered in our visa gift card giveaway: https://linktr.ee/mybestfriendsanengineer

How is CTE different from a concussion?  Neil deGrasse Tyson and co-hosts Chuck Nice and Gary O'Reilly discuss concussions and chronic traumatic encephalopathy, with former NFL lineman, Leonard Marshall, and neuroscientist, Heather Berlin, PhD.NOTE: StarTalk+ Patrons can watch or listen to this entire episode commercial-free.Thanks to our Patrons Walter Johnson, Ali AlWaheedy, Armen Gevorgyan, Jenny K Leasure, WIGwigWIG, Denny, MaKayla A Holloway, Anna Dupre-Whiting, Allain Brideau, and David for supporting us this week.Photo Credit: Garpenholm, CC BY-SA 3.0, via Wikimedia Commons

In the fifth episode of The Alzheimer's Solutions Revolution podcast with Ralph Sanchez, I talk with my co-host Susan Brender, as we continue with our special podcast series called Think Ahead. In this week's episode, I'll provide an overview on the role of tau protein and neurofibrillary tangles (tau tangles) in the progression and development of late-onset Alzheimer's disease (LOAD). The toxic accumulation of tau tangles in brain cells (neurons) are one of the two hallmark lesions associated with Alzheimer's disease (AD). The aggregation of beta-amyloid peptides (protein) into amyloid plaque is the other toxic hallmark lesion linked to the onset and progression of LOAD. Additionally, I'll give an a summary on the importance that tau protein plays in a critical component in the conveyance network and cytoskeletal structure that is an essential element of neuronal function and structure. The cytoskeletal conveyance structure of the neuron contributes to the shuttling of mitochondria to the neurons axonal terminal and synapse in order to provide the energy metabolism required for synaptic function. Please listen in and be informed! Ralph Sanchez, MTCM, CNS, D.Hom www.TheAlzheimersSolution.com https://www.facebook.com/TheAlzheimersSolution https://www.linkedin.com/in/ralph-sanchez https://www.instagram.com/alzheimers_solution

Tickled by tau? Preoccupied with post-translational modifications? Join Kate as she covers the latest papers published in December 2021 on tau protein pathology and targeting tau as a therapeutic strategy in Alzheimer's disease.  Sections in this episode:  Tau Aggregation & Post-Translational Modifications (3:19)  Generalized Tau Pathology & Tau Seeding (7:29)  Treatments Targeting Tau in AD (13:50) -------------------------------------------------------------- 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/1fjqrnVxElJ6O3DpCytRflRFP0Td_Vg51/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 Kate Van Pelt, edited by Chihiro Abe, and reviewed by Alyssa Ash and Ellen Koch. The bibliography was made by Anjana Rajendran 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!" 

Join Kate for a comprehensive summary of everything tau from papers published in November 2021.  We'll talk post-translational modifications, prion-like seeding pathology, molecular modeling, and even touch on a potential AD therapies targeting this fascinating little microtubule helper. Enjoy! :)  Sections in this episode:  Tau Aggregation and Post-Translational Modifications (03:03)  Tau Seeding and General Tau Pathology (12:49)  Novel Therapeutics (22:58) -------------------------------------------------------------- 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/1bN5cizXqwbfTb-zaQsSckYjMcyz75kzF/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 Kate Van Pelt, edited by Lara Onbasi, and reviewed by Alyssa Ash and Anusha Kamesh.  The bibliography was made by Anjana Rajendran, 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!" 

Kate lets you know what's going on in the world of tau protein research in this episode of AMiNDR! Tune in to hear all about tau seeding, tau pathology, and potential therapeutic interventions for Alzheimer's Disease that target this protein. Enjoy!  Sections in this episode:  Tau seeding-related pathology (3:40)  Targeting tau for therapeutic interventions in AD (14:35) -------------------------------------------------------------- You can find the numbered bibliography for this episode by clicking here, or the link below:https://drive.google.com/file/d/1-KRBJQRI7Z9e0EjmqqlZUPYHv34rkUlU/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 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 leaving us a review on Apple Podcasts 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 Kate Van Pelt, edited by Chihiro Abe,  and reviewed by Alyssa Ash and Anusha Kamesh. The bibliography and wordcloud were 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 October 2021, the sorters were Jacques Ferreira, Christy Yu, Kate Van Pelt, Eden Dubchak, Kira Tosefsky, Dana Clausen, 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, and Shruti Kocchar 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!" 

Tired of untangling the tricky world of tau literature all on your own? Interested in the mechanisms of tau pathology, therapeutic advancements targeting tau, or both? Join Kate for another exciting episode covering 20 new papers published in September 2021. We'll explore tau aggregation, regulation, and treatment development through a wide variety of model systems, from molecular dynamics all the way to human subjects - so, tune in to learn more!  Sections in this episode:  New tau pathological findings (3.17)  Tau and Neuroinflammation (7.46)  Tau Aggregation (10.24)  Tau Pathology from Prion-like Seeding Behaviour (13.24)  Treatments Targeting Tau (24.59) -------------------------------------------------------------- You can find the numbered bibliography for this episode by clicking here, or the link below:https://drive.google.com/file/d/1fEz6EzLv2f8OpLYPQ6RsQKkgM2hFwVwX/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 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 leaving us a review on Apple Podcasts 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 Kate Van Pelt, edited by Anusha Kamesh, and reviewed by Sarah Louadi and Ellen Koch. The bibliography was made by Anjana Rajendran and the wordcloud 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 September 2021, the sorters were Jacques Ferreira, Ellen Koch, Christy Yu, Sarah Louadi, Kate Van Pelt, Nicole Corso, Eden Dubchak, Kira Tosefsky, Dana Clausen, and Elyn Rowe.Also, props to our management team, which includes Sarah Louadi, Ellen Koch, Naila Kuhlmann, Elyn Rowe, Anusha Kamesh, Jacques Ferreira, and Shruti Kocchar 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!" 

This episode is also available as a blog post: https://mdforlives.blog/2021/10/11/abnormal-tau-protein-hallmark-indicator-of-alzheimers-disease/ --- Send in a voice message: https://anchor.fm/mdforlives/message

Today, Kate will be focusing on everything tau-related in 12 papers published in August 2021, including aspects of tau pathology and exploring potential therapeutics targeting tau in Alzheimer's disease! Sections in this episode:Tau Aggregation & Post-Translational Modifications (PTMs) (3.16)Tau Pathology & Seeding (13.30)Targeting Tau for Treatment (20.10)-------------------------------------------------------------- You can find the numbered bibliography for this episode by clicking here, or the link below:https://drive.google.com/file/d/1IIilzUhWAF_WuBM4trkcW12daiB52sT2/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 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 leaving us a review on Apple Podcasts 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 together to bring you every episode of AMiNDR. In particular, this episode was scripted and hosted by Kate Van Pelt, edited by Sarah Louadi, and reviewed by Ellen Koch. The bibliography was made by Anjana Rajendran and the wordcloud was created by Sarah Louadi (www.wordart.com). Big thanks to the sorting team for sorting all the papers published in August 2021 into themes for our episodes: Jacques Ferreira, Ellen Koch, Nicole Corso, Kate Van Pelt, Christy Yu, Dana Clausen, Kira Tosefsky, and Eden Dubchak.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, 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!" 

Kate brings you the latest research on tau pathology in Alzheimer's Disease. This includes post-translational modifications, tau aggregation and seeding, and targeting tau in treatment development. Enjoy!   Sections in this episode:  Tau Pathology (4:35)  Post-translational modifications (4:56)  Tau aggregation and seeding behaviour (16:30)  Targeting Tau for Treatment Development (21:09)  -------------------------------------------------------------- You can find the numbered bibliography for this episode by clicking here, or the link below:https://drive.google.com/file/d/1xBMvUdqdBPnGQDnv9qBk9icbKBNEbdXZ/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. It helps us a lot and we thank you in advance for leaving a review! Every episode of AMiNDR is the result of a huge team effort. Today's episode was scripted and hosted by Kate Van Pelt, edited by Michelle Grover, and reviewed by Ellen Koch and Sarah Louadi. The wordcloud (wordart.com) was generated by Sarah Louadi and the bibliography was created by Lara Onbasi.  Big thanks to the sorting team for sorting all the papers published in July 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!" 

Today my guest is Pathology PhD Candidate Kimberly Fiock What we discuss with Kimberly: The differences between a Pathology PhD and a Pathologist How a neuropathology internship led to her interest in pathology Her research in tau protein as part of her Masters degree work The Iowa Neurobank Core and her role there Some of her creative and volunteering activities Her Instagram page and how she uses it to educate others about pathology Why it is important to acknowledge burnout and some things we can do about it Links for this episode: Health Podcast Network  LabVine Learning The ConfLab from LabVine Dress A Med scrubs   Kimberly Fiock: Twitter Instagram Iowa Neurobank Core Increased Tau Expression Correlates with Neuronal Maturation in the Developing Cerebral Cortex   People of Pathology Podcast: Website Twitter

Will mutations change our vaccination strategy? Also, a controversial step in the fight against Alzheimer's, and how to tell a six-year-old what a quantum computer is.

In this episode, Marcia will cover papers published in Sept 2020 on treatment development for AD with special focus on the tau protein. She discusses tau in its role as a microtubule-associated protein and the related use of microtubule-stabilizing agents in treating AD. She also talks about papers on immunotherapy, autophagy, and inhibiting tau hyperphosphorylation. Tune in to hear about all of this and more! ------------------------------------------------------------------  To receive the list of papers covered, please fill this form:  -------->  https://forms.gle/CVVbznAFM8pamdgk6  -------  or by tweeting 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.podcast------------------------------------------------------------------ Today's episode was scripted and hosted by Marcia Jude, reviewed by Elyn Rowe, and edited by Yvonne Deng. Big thanks to Elyn Rowe and Jacques Ferreira for sorting all the papers published in September into themes for our episodes, and props to the team that works very hard behind the scenes to make all this possible. 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!"  

Alyssa will cover tau protein expression, aggregation, and pathology in Alzheimer's Disease from studies published in Sept 2020. This episode will dive into papers that examine genetic mutations, toxin exposure and protein interactions that lead to tau pathology and identify potential future therapeutic targets to treat these diseases. A quickie but a goodie if learning more about tau protein is your jam! ------------------------------------------------------------------ To receive the list of papers covered, please fill this form:  -------->  https://forms.gle/CVVbznAFM8pamdgk6  -------  or by tweeting 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.podcast------------------------------------------------------------------ Today's episode was scripted and hosted by Alyssa Ash, reviewed by Ellen Koch, and edited by Sanjana Bedi and Anusha Kamesh. All of this was made possible thanks to 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!  Joseph tells you about more papers on drugs in development from June 2020.   These studies encompass those done in vitro or using computational models, but not animal testing. Here, you will hear about approaches with multiple targets: cholinesterase, amyloid-beta, tau, oxidative stress...  If you're interested in hearing more about treatments for AD, you should also check out our episodes on pre-clinical and clinical testing.  To receive the list of papers covered (with timestamps), please fill this form: -------->  https://forms.gle/CVVbznAFM8pamdgk6  ------- or by tweeting 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/5aq2JyrT6g4P1m8v6You can also share your thoughts and suggestions by contacting us: Email: amindrpodcast@gmail.com Facebook:  AMiNDR Twitter: @AMiNDR_podcast*New* Instagram: @AMiNDR.podcast----------------------------------------------------------------------- Today's episode was scripted and hosted by Joseph Len Liang-Lee, edited by Sarah Louadi, 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!  Ellen tells you about more papers on drugs in development from June 2020.   These studies encompass those done in vitro or using computational models, but not animal testing. This time around, she will be focusing on papers where the target is tau protein, the cholinergic system, metabolism, mitochondria, neuroinflammation, and autophagy from June 2020! If you're interested in hearing more about treatments for AD, you should also check out our episodes on pre-clinical and clinical testing.  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: (2:14)      Targeting tau          (10.13)    Targeting the cholinergic system(20:56) Targeting metabolism(22:05) Targeting the immune system / neuroinflammation / glia(24.45) Targeting mitochondria and/or oxidative stress(30.32) Targeting autophagy----------------------------------------------------------------------- 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.com Facebook:  AMiNDR Twitter: @AMiNDR_podcast*New* Instagram: @AMiNDR.podcast----------------------------------------------------------------------- Today's episode was scripted by Mahraz Parvand & Joseph Len Liang-Lee, hosted & edited by Ellen Koch, 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: (1.09) Neuroinflammation/glial cells(14.40) Protein aggregation and post-translation modification (eg: phosphorylation, misfolding), protein-protein interactions(33.31) Cell metabolism (mitochondrial dysfunction, lipids, hormones)(39.00) Neuronal plasticity : cell proliferation, differentiation, maturation, survival + cell death + survival/protection(42.11) Cerebrovascular changes(45.49) Synaptic Transmission(54.33) Autophagy This episode was curated and produced by a group of volunteers. As we work on producing full-length episodes on ALL the publications from May 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.  Email: amindrpodcast@gmail.comTwitter: @AMiNDR_podcast *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: Methods and Models, Risk Factors/Genetics & Biomarkers/Diagnosis, Treatments and Testing, Miscellaneous.

The very first girl on the podcast, who undoubtedly drops the STEM is Allison Jia! At ISEF she received the Intel Foundation Young Scientist Award of US$50,000 for her outstanding research into toxic tau protein aggregates, which spread in neurons in the human brain and are associated with neurodegenerative diseases such as Alzheimer’s. She is the president of the Society for Neuroscience - Bay Area’s Chapter, and is passionate about promoting scientific discoveries. Allison tickles the ivories and serves strong on the volleyball court, too! https://www.instagram.com/dropthestempodcast/ Music Credit: https://www.purple-planet.com

On this weeks episode of the podcast Matt sat down and spoke with Professor Tim Lynch. Tim is the director of The Dublin Neurological Institute at the Mater Hospital as well as being a Consultant Neurologist. On the show Tim speaks about Alzheimer's, Dementia, Tau Protein, The Brain, How to look after your brain and so much more! Huge thank you to Tim for coming onto to the show it was really insightful and educational talk for us all. If you would like to know more about Tim’s work and would like to donate please visit - https://www.neurologicalinstitute.ie Special thanks to our: Sponsors: Niall Reilly- www.rooneymedia.com Carolyn Harvey- ISA Nutrition. Magic Minds Podcast Team Matt Burke- Host Kevin Doyle- The Technical Legend Aaron Keogh- Social Media & Promotion --- Send in a voice message: https://anchor.fm/magic-minds/message

Adam Boxer offers an overview of the latest on diagnosis and treatment for progressive supranuclear palsy.

Progressive supranuclear palsy (PSP) is a condition that affects the brain with symptoms that worsen over time. Irene Litvan, MD joins William Mobley, MD, PhD to talk about the signs and symptoms of PSP, disease progression, genetic issues, as well as potential treatments on the horizon. Series: "Women in Science" [Health and Medicine] [Science] [Show ID: 30399]

Progressive supranuclear palsy (PSP) is a condition that affects the brain with symptoms that worsen over time. Irene Litvan, MD joins William Mobley, MD, PhD to talk about the signs and symptoms of PSP, disease progression, genetic issues, as well as potential treatments on the horizon. Series: "Women in Science" [Health and Medicine] [Science] [Show ID: 30399]

Thu, 16 Jan 2014 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/16578/ https://edoc.ub.uni-muenchen.de/16578/1/Mehle_Anja.pdf Mehle, Anja

Ziel der vorliegenden Arbeit war es, einen neuen Wirkstoff für die Therapie des Morbus Alzheimer zu entwickeln. Morbus Alzheimer ist die häufigste Demenzerkrankung in Deutschland (1). Charakteristisch für diese neurodegenerative Erkrankung ist die zu-nehmende Verschlechterung der kognitiven Leistungsfähigkeit, die mit einem Untergang von Nervenzellen und Synapsen einhergeht. Für die neuropathologische Diagnose des Morbus Alzheimer ist der Nachweis von extrazellulären Aβ-Plaques und intrazellulären versilberbaren Strukturen, den sogenannten neurofibrillären Bündeln (tangles) entscheidend (5). Die Enzyme, die zu der Bildung dieser Aggregate, die im Wesentlichen aus fehlgefalteten körpereigenen Proteinen, dem β-Amyloid bzw. dem Tau-Protein bestehen, beitragen, sind die primären Zielmoleküle in der Wirkstoffentwicklung auf diesem Gebiet in den letzten 20 Jahren gewesen. So wurde eine große Zahl von Wirkstoffen bzw. thera-peutischen Ansätzen identifiziert, die effektiv in vitro und in vivo die Bildung dieser Aggregate inhibieren (1). Die erhofften Effekte auf die alters- und amyloid-abhängigen Defizite bei der Lern- und Gedächtnisleistung konnten durch klinische Studien jedoch nicht belegt werden (73). Eine mögliche Erklärung für den Misserfolg dieser sehr auf-wändigen Studien ist, dass Veränderungen durch Ablagerungen von fibrillärem Aβ bzw. Tau zu irreversiblen Schädigungen führen und somit eine ausschließlich auf Aβ- bzw. Tau fokussierte Therapie nach Ausbruch der Krankheit möglicherweise nicht ausrei-chend ist. Mit den in der Arbeitsgruppe etablierten zellbasierten Assays ist es möglich, Wirkstoffe zu identifizieren, die die Störung der Speicherung von Kalzium im endoplasmatischen Retikulum (ER), einen pathophysiologisch relevanten Mechanismus der Pathogenese des Morbus Alzheimer, modulieren (120). Dieser Ansatz verfolgt somit nicht die seit Jahren praktizierte Strategie, die Aβ- bzw. Tau-Aggregation direkt zu hemmen, sondern der für die Akkumulation dieser Proteine ursächlichen Schädigung von Nervenzellen und deren synaptischen Kontakten entgegenzuwirken. Ziel war es, innovative Wirkstoffe zu entwickeln, die Störungen der zytosolischen Kalziumkonzentration bzw. der Kal-ziumfreisetzung aus dem ER in einer frühen Phase der neuronalen Schädigung normali-sieren. Optimierte Vertreter der neu entdeckten Strukturklasse der Tetrahydrocarbazolamine stabilisieren in der Tat die Kalziumfreisetzung aus dem ER, verbessern den Energiehaushalt der Zelle und verringern die Bildung toxischer Aβ-Peptide. Der genaue Wirkmechanismus der Tetrahydrocarbazolamine konnte in dieser Arbeit jedoch nicht entschlüsselt werden und wird Gegenstand zukünftiger Forschungs-projekte sein müssen. Als mögliches Target bieten sich zum Beispiel IP3-Rezeptoren an. Eine mögliche Interaktion mit diesen könnte dazu führen, dass weniger Kalzium aus dem endoplasmatischen Retikulum in das Zytosol austritt. Die identifizierten Verbindungen haben zusätzlich einen positiven Effekt auf die Aktivität der Mitochondrien, was wiederum zu einer Steigerung der Energiebereitstellung der Zelle führt und einen Effekt auf die Produktion von Aβ-Peptiden hat (56). Auch Kalzium beeinflusst über eine indirekte Hemmung der β-Sekretase die Menge an gebildetem Aβ (157). In Folge dessen wirken Tetrahydrocarbazolamine sehr wahrscheinlich über verschiedene Mechanismen auf die Bildung der toxischen Aβ-Peptide. Eine synergistische Verstärkung ist daher durchaus denkbar. Tetrahydrocarbazolamine besitzen somit eine Wirkung auf drei verschiedene Mechanismen, die bereits zu Beginn der Pathogenese von Morbus Alz-heimer eine wichtige Rolle spielen. Zurzeit befinden sich nach den uns zugänglichen Informationen keine anderen Substanzen in der präklinischen oder klinischen Entwick-lung, die ein ähnlich breites Wirkprofil aufweisen. In den anschließend durchgeführten Therapieversuchen in transgenen Mausmodellen des Morbus Alzheimer konnte allerdings kein Effekt auf die Anzahl und Größe von Plaques festgestellt werden. Dies ist vermutlich vor allem der kurzen Behandlungsdauer zuzuschreiben. Eine längere Behandlung mit gea_133 war auf Grund einer Lebertoxizität, die wahrscheinlich ursächlich für das Sterben der Tiere in der 3. Behandlungswoche war, nicht möglich. Ein zentraler Punkt der zukünftigen Erforschung dieser Substanzklasse wird die Entwicklung und Testung von Derivaten sein, die keine Lebertoxizität aufweisen.

Aims: In this study, we aimed to compare cerebrospinal fluid (CSF) levels of total tau (t-tau), phosphorylated tau (p-tau(181)) and positron emission tomography with F-18-fluorodeoxyglucose (FDG-PET) in the differential diagnosis of Alzheimer's disease (AD) under clinical conditions. Method: In a cross-sectional, blinded, single-center study, we examined a sample of 75 unselected memory clinic patients with clinical diagnoses of dementia of Alzheimer type (DAT; n = 24), amnestic mild cognitive impairment (MCI; n = 16), other dementias (n = 13) and nondemented controls (n = 22). Discriminative accuracy, sensitivity and specificity were calculated and compared using ROC analyses. Results: p-tau(181) and FDG-PET were comparable in separating DAT from controls (sensitivity: 67 vs. 79%; specificity: 91% for both) and patients with other dementias (sensitivity: 71 vs. 79%; specificity: 100% for both). The sensitivity of p-tau 181 in differentiating MCI patients from controls was significantly (p < 0.05) superior to that of FDG-PET (75 vs. 44%) at a comparably high specificity (82 vs. 91%); t-tau measures were less accurate in all analyses. Conclusions: FDG-PET and CSF p-tau(181) levels are able to discriminate DAT in heterogeneous and unselected samples with a high accuracy. CSF p-tau(181) might be somewhat superior for a sensitive detection of patients with MCI. Copyright (C) 2010 S. Karger AG, Basel

Die Alzheimer-Krankheit (AD), die häufigste Form der Demenz, manifestiert sich klinisch meist ab dem 65. Lebensjahr mit langsam progredienten Gedächtnis-, Orientierungs- und Aufmerksamkeitsstörungen. Neuropathologische Korrelate sind die Amyloid-Plaques, die hauptsächlich aus extrazellulären Aggregaten des β-Amyloid-Proteins (Aβ) zusammengesetzt sind, und intrazelluläre neurofibrilläre Bündel, die aus Aggregaten des mikrotubulus-assoziierten Proteins Tau bestehen. Der „Auslöser“ der Alzheimer-Krankheit ist das β-Amyloid-Protein (Amyloid-Kaskaden-Hypothese), welches durch proteolytische Prozessierung von βAPP (β-Amyloid-Vorläufer-Protein) entsteht. Dies geschieht, indem zuerst BACE-1 (β-site APP cleaving enzyme 1) und anschließend der γ-Sekretase-Komplex βAPP schneiden. Menschen mit Down-Syndrom (DS), welches die häufigste autosomale Chromosomenaberration darstellt, entwickeln bereits ab einem Alter von 40 Jahren die typischen neuropathologischen Kennzeichen der Alzheimer-Krankheit und zeigen mit einem Durchschnittsalter von 56 Jahren die klinischen Symptome der Demenz. Die Gründe für das frühe Auftreten der Amyloid-Plaques sind noch nicht vollständig geklärt. Das Gen für βAPP befindet sich auf dem Chromosom 21, welches im DS dreifach vorhanden ist, und wird daher mit der frühen Plaque-Pathologie im Down-Syndrom in Zusammenhang gebracht. BACE-1 konnte durch Überexpressions- und Knock-out-Experimente eindeutig als alleinige β-Sekretase identifiziert werden. In Gehirnen von Alzheimer-Demenz-Patienten konnten im Vergleich zu Kontrollgehirnen erhöhte BACE-1-Proteinmengen und BACE-1-Aktivitäten nachgewiesen werden. Es war deshalb interessant zu untersuchen, ob auch im Gehirn von Down-Syndrom-Patienten die BACE-1-Proteinexpression erhöht ist. Durch eine Hochregulation von BACE-1 im Down-Syndrom könnte vermehrt βAPP prozessiert und somit Aβ gebildet werden. Daher war es das Ziel der vorliegenden Arbeit die Expression von BACE-1 in Gehirnen (Temporal- und Frontallappen) von DS-Patienten im Vergleich zu Kontrollgehirnen zu analysieren. In der Western-Blot-Analyse der Gewebeproben konnte gezeigt werden, dass die BACE-1-Proteinmengen im Down-Syndrom im Vergleich zu den Kontrollen (K) 1,4-fach erhöht waren. Die Proteinexpressionen von βAPP zeigten sich im DS im Vergleich zu den Kontrollen 1,4-fach erhöht. Diese Ergebnisse erzielten keine Signifikanz, zeigten aber deutliche Trends im Expressionsverhalten. Dies könnte auf die Anzahl der untersuchten Gehirne (Temporal- und Frontallappen je 3 DS, 4 AD und 5 K), Qualitätsmängel der Gehirnproben oder einer ungleichen Verteilung der Proteinexpression im Gewebe zurückzuführen sein. Es ist daher notwendig mehr Gehirne zu untersuchen. Zudem wäre es interessant in Gehirnschnitten das Verteilungsmuster der BACE-1-Expression im DS genauer zu studieren. Die Ergebnisse deuten jedoch auf eine Hochregulation von BACE-1 im DS-Gehirn und somit auf eine Beteiligung der Protease an der Plaquepathologie des Down-Syndroms hin. BACE-1 scheint also sowohl in der Pathogenese der Alzheimer-Demenz als auch in der des Down-Syndroms eine zentrale Rolle einzunehmen. Daher ist es sehr interessant die Regulation von BACE-1 weiter zu analysieren. Da in p25-überexprimierenden Mäusen erhöhte BACE-1-Proteinexpressionen gezeigt werden konnten, vermutete man eine Beteiligung von p25 an der Regulation der β-Sekretase. p25, das im Gehirn der AD-Patienten vermehrt gebildet wird und aus der Proteolyse von p35 entsteht, bindet und aktiviert die Kinase cdk5. cdk5 phosphoryliert unter anderem das Tau-Protein und wird daher mit der Bildung der neurofibrillären Bündel in Zusammenhang gebracht. Durch die Hochregulation von BACE-1 könnte p25 in der Pathogenese der Alzheimer-Erkrankung eine neue Bedeutung zugeschrieben werden. Zur Analyse der p25 induzierten Veränderungen in den Neuronen wurden humane Neuroblastomazellen mit einem induzierbaren p25-Expressionsvektor, Sp25-Zellen, verwendet. In diesen p25-überexprimierenden Zellen konnten sowohl in der Western-Blot-Analyse als auch in der BACE-1-Aktivitätsmessung erhöhte BACE-1-Proteinexpressionen bzw. BACE-1-Aktivitäten gezeigt werden. Die Northern-Blot-Analyse der Sp25-Zellen ergab erhöhte BACE-1-mRNA-Spiegel, die sich jedoch in einer für endogene BACE-1-mRNA untypische Größe detektieren ließen. p35, das membrangebundene Vorläufer-Protein von p25, war indes nicht in der Lage die BACE-1-Proteinexpression in humanen Neuroblastomazellen zu erhöhen. Die Ergebnisse der Sp25-Zellen konnten in p25-überexprimierenden murinen Neuroblastomazellen, Np25-Zellen, nicht reproduziert werden. Daher ist es notwendig, den p25-induzierten BACE-1-Regulationsmechanismus auf seine Reproduzierbarkeit, z.B. in weiteren In-vivo-Modellen, zu überprüfen.

Die Synucleinopathien sind eine Gruppe neurodegenerativer Erkrankungen, die durch pathologische Ablagerungen des Alpha Synucleins charakterisiert sind. Sie umfassen unter anderem den Morbus Parkinson, die Demenz mit Lewy-Körperchen, die multiple Systematrophie und die Lewy Körperchen Variante des auch durch Ablagerungen des Tau Proteins gekennzeichneten Morbus Alzheimer. Ziel der vorliegenden Arbeit war die Analyse von Aggregationsprozessen des Alpha Synucleins durch einzelmolekülspektroskopische Verfahren und die Entwicklung neuer Techniken zur Analyse von Koaggregationsprozessen verschiedener Proteine. Hierzu wurden Synuclein und Tau Proteine rekombinant in E. coli hergestellt, aufgereinigt, durch Gelelektrophorese und Western Blot charakterisiert und Aggregationsprozesse unter in vitro Bedingungen untersucht. Rekombinantes Alpha Synuclein kann unter bestimmten Bedingungen in vitro zu fibrillären, amyloiden Strukturen aggregieren. Diese Aggregate ließen sich durch eine spezifische Änderung der Thioflavin T Fluoreszenz spektroskopisch nachweisen, mittels Elektronenmikroskopie darstellen, und zeichneten sich durch partielle Resistenz gegen die Einwirkung der Serin Protease Proteinase K aus. Durch Einbau von homologen Sondenmolekülen, die zuvor mit einer fluoreszenten Gruppe kovalent konjugiert wurden, ließ sich die Fibrillenbildung auch mit einzelmolekülbasierten, konfokalen, fluoreszenzspektroskopischen Analyseverfahren wie der Kreuzkorrelationsanalyse und der SIFT-Methode (engl. Scanning for Intensely Fluorescent Targets) darstellen. Der Nachweis der Fibrillenbildung war durch die fluoreszenzspektroskopischen Verfahren 100 fach sensitiver möglich. Im Vergleich mit nicht amyloidogenen Proteinen wie Beta Synuclein und Serum Albumin konnte zudem die Spezifität der Aggregation gezeigt werden. Bei neurodegenerativen Erkrankungen findet sich zum Teil die Beteiligung mehrerer amyloidogener Proteine am pathologischen Prozess. Durch die Möglichkeit der simultanen Anregung verschiedener Fluoreszenzsonden bei verschiedenen Wellenlängen und der Differenzierung des emittierten Fluoreszenzsignals konnten Koaggregationsprozesse in heterogenen Systemen mit Hilfe der Einzelmolekülspektroskopie untersucht werden. Es zeigte sich, dass Alpha Synuclein sowohl mit seinem Maushomolog, als auch mit den beiden humanen Parkinson-assoziierten Mutanten A30P und A53T gemischte Fibrillen bildet, während Beta Synuclein einen hemmenden Einfluss auf die Alpha Synuclein Fibrillenbildung aufwies. Mit Hilfe des zweifarbigen Systems ließ sich auch der Anlagerungsprozeß von Alpha Synuclein Monomeren an vorbestehende, amyloide Alpha Synuclein Aggregate darstellen, was einen weiteren Einblick in die molekulare Pathophysiologie der Synucleinopathien bot. Es wird vermutet, dass bereits Oligomerformationen einen neurotoxischen Effekt besitzen. Die besondere Sensitivität der konfokalen Einzelmolekülspektroskopie erlaubte ebenfalls die Detektion von frühen oligomeren Aggregaten des Alpha Synucleins sowie des Tau Proteins. Es konnte gezeigt werden, dass Alpha Synuclein bereits auf Oligomerebene heterogene Aggregate mit dem Tau Protein bildet, was durch die Tatsache, dass es sich bei beiden um intrazelluläre Proteine handelt, eine potentielle pathophysiologische Relevanz besitzt. Im Rahmen von Versuchsreihen zum Einfluss von Liquor aus an verschiedenen neurodegenerativen Erkrankungen leidenden Patienten, ließen sich Hinweise auf eine mögliche neuroprotektive Funktion des Liquors gewinnen. Dieser zeigte nach Gelfiltration in bestimmten Fraktionen deutlich aggregationshemmende Eigenschaften. Diese Fraktionen besitzen einen hohen Gehalt an Albumin. Zusammen mit in vitro gewonnenen Daten, die einen hemmenden Einfluss von Albumin auf die Aggregation des Alpha Synucleins zeigen, sind dies Hinweise, dass die protektive Eigenschaft an den Albumingehalt des Liquors gekoppelt ist. Das diagnostische Potential der entwickelten Messmethode verdeutlichten parallel durchgeführte Analysen von Influenza-Impfstoffpräparationen, in denen gezeigt werden konnte, dass sich Partikel mit unterschiedlichen Oberflächenepitopen auch in Mischungen differenzieren lassen. Durch den Einsatz von spezifischen fluoreszenzmarkierten Antikörpern ließen sich eindeutig bestimmte Influenzastämme anhand der Oberflächenepitop-Konfiguration identifizieren. Zusammenfassend konnte gezeigt werden, dass die konfokale Einzelmolekülspektroskopie eine äußerst sensitive und hochdurchsatzfähige Nachweismethode zur Untersuchung der molekularen Vorgänge im Rahmen der Alpha Synucleinopathien darstellt, deren Potential sich nicht allein auf die Grundlagenforschung beschränkt, sondern auch diagnostische Möglichkeiten beinhaltet und eine neue Methode zur Suche von bisher noch nicht beschriebenen, pharmakologisch interessanten Strukturen bietet.

Background: S-100B and tau protein have a high differential diagnostic potential for the diagnosis of Creutzfeldt-Jakob disease (CJD). So far there has been only limited information available about the dynamics of these parameters in the cerebrospinal fluid (CSF). However, there is a special interest in finding biochemical markers to monitor disease progression for differential diagnosis and treatment. Patients and Methods: We analyzed CSF of 45 patients with CJD and of 45 patients with other neurological diseases for tau protein and S-100B in a follow-up setting. All diagnoses of CJD were later neuropathologically verified. A ratio between tau protein differences and the time between lumbar puncture was calculated. The same was done for S-100B. Results: Tau protein levels of 34 cases were above the cut-off level for CJD (>1,300 pg/ml) in the first CSF sample. In 7 of 11 patients with lower tau levels in the first CSF sample, tau levels rose. The above-mentioned ratio was significantly higher in the CJD group than in the group with other neurological diseases. Similar results were obtained for S-100B. Conclusion: We conclude that follow-up investigations and calculation of ratios is a useful tool in the differential diagnosis of CJD. Variations in this pattern were observed in single cases. Copyright (C) 2005 S. Karger AG, Basel.

The intra vitam diagnosis of dementia with Lewy bodies (DLB) is still based on clinical grounds. So far no technical investigations have been available to support this diagnosis. As for tau protein and beta-amyloid((1-42)) (Abeta42), promising results for the diagnosis of Alzheimer's disease ( AD) have been reported; we evaluated these markers and S-100B protein in cerebrospinal fluid (CSF), using a set of commercially available assays, of 71 patients with DLB, 67 patients with AD and 41 nondemented controls (NDC) for their differential diagnostic relevance. Patients with DLB showed significantly lower tau protein values compared to AD but with a high overlap of values. More prominent differences were observed in the comparison of DLB patients with all three clinical core features and AD patients. Abeta42 levels were decreased in the DLB and AD groups versus NDC, without significant subgroup differences. S-100B levels were not significantly different between the groups. Tau protein levels in CSF may contribute to the clinical distinction between DLB and AD, but the value of the markers is still limited especially due to mixed pathology. We conclude that more specific markers have to be established for the differentiation of these diseases. Copyright (C) 2005 S. Karger AG, Basel.

Tau ist ein Mikrotubuli- assoziiertes Protein, dessen Expression im Nervensystem des Menschen der Regulation durch alternatives Spleißen unterliegt. Das Exon 10 dieses Gens, welches für einen Teil der Mikrotutuli- bindenden Domäne kodiert, ist ein für Erwachsene spezifisches Kassettenexon. Mutationen, die den Einschluss von Exon 10 verstärken, resultieren in der Produktion von Tau- Protein, das vier Mikrotubuli- bindende Aminosäuresequenzwiederholungen enthält. Diese Mutationen scheinen in ursächlichem Zusammenhang mit der Frontotemporalen Demenz mit Parkinsonismus gekoppelt an Chromosom 17 (FTDP- 17) zu stehen. In dieser Arbeit konnte mittels Transfektionsexperimenten gezeigt werden, dass die Verwendung von Exon 10 durch ein komplexes Zusammenspiel der CDC- ähnlichen Kinase Clk2, einer SR- Proteinkinase, und des SR- ähnlichen Proteins humaner Transformer 2- b (Htra2- b) reguliert wird. Kotransfektionsexperimente legen den Schluss nahe, dass diese Regulation über mehrere ineinandergreifende Prozesse abläuft. Die Kinase Clk2 scheint dabei sowohl direkt durch Posphorylierung bzw. Hyperphosophorylierung von Htra2- b als auch indirekt durch Einfluss auf die alternative Expression der Htra2- b Isoformen in den Regulationsmechanismus einzugreifen. Phosphorylierung von SR- Proteinen führt zu deren Freisetzung aus den nukleären Speicherkomponenten, den speckles, und damit zur Aktivierung der Spleißreaktion, während sowohl eine Hyper- als auch eine Hypophosphorylierung in der Regel einen hemmenden Einfluss auf Spleißen ausüben. Kontrollierte Phosphorylierung scheint demnach zu einer regulierbaren Veränderung von prä- mRNA- Prozessierungswegen zu führen. Eine Interpretation dieser Resultate könnte als Grundlage für die Entwicklung neuer therapeutischer Konzepte verwendet werden.