Podcasts about synapsin

In today's episode, host Chris Duffin dives deep into the fascinating world of cognitive enhancement with special guest Anthony Castor. We'll explore a range of nootropic peptides and supplements designed to boost brain function, resilience, and overall well-being. Chris and Anthony discuss such potent peptides as C Max and Celnac, revealing their roles in cognitive enhancement, neuroprotection, and stress resistance. We'll learn about Synapsin's ginsenoside RG3, and its anti-aging properties, and the intriguing nootropic properties of NewPEPT. Listen as Anthony shares personal anecdotes about using compounds like Dihexa for synapse formation and modafinil for enhancing wakefulness and cognitive performance. Throughout the conversation, we'll also delve into the science behind these compounds, examining their neurotransmitter modulation, neuroprotection, and practical applications for high-stress jobs, shift work, and productivity boosts. Additionally, we'll cover lifestyle practices that complement these cognitive enhancers, emphasizing the importance of sleep, hydration, and a balanced diet.   This episode of the ARCHITECT of RESILIENCE podcast is available on Apple, Spotify & YouTube, and is sponsored by  @marekhealth : Performance. Longevity. Optimization.

View the Show Notes For This Episode Dr. James Lavalle discusses Metaflammaging with Dr. Ben Weitz. [If you enjoy this podcast, please give us a rating and review on Apple Podcasts, so more people will find The Rational Wellness Podcast. Also check out the video version on my WeitzChiro YouTube page.] Podcast Highlights In this episode of the Rational Wellness Podcast, host Dr. Ben Weitz engages in a comprehensive discussion with Dr. James LaValle, an internationally recognized clinical pharmacist and nutritionist. They delve into the concept of metaflammation—metabolic inflammation—and its impact on health and aging. Dr. LaValle shares his personal journey into integrative and functional medicine, his work with athletes and professional teams, and his development of the Metabolic Code. He also discusses the significance of various biomarkers for assessing health, the role of GLP-1 agonists in obesity and diabetes management, and the potential benefits and concerns surrounding peptides. Additionally, they cover the importance of lifestyle changes, stress management, and innovative health technologies in promoting longevity and well-being.   00:00 Introduction to the Rational Wellness Podcast 00:29 Meet Dr. James LaValle: A Journey in Integrative Medicine 05:26 The Metabolic Code and Personalized Care 06:33 The Role of Lifetime in Promoting Wellness 07:31 Understanding Biomarkers and Metabolic Health 18:02 The Impact of GLP-1s and Lifestyle Changes 27:12 Concerns and Considerations with GLP-1s 31:05 Inflammation Markers: Mean Platelet Volume and Neutrophil Lymphocyte Ratio 31:42 Understanding Metabolic Inflammation 32:09 The Role of Basophils and Cortisol in Inflammation 32:25 Neutrophils, Lymphocytes, and Immune System Stress 33:27 Monocytes and Macrophages: Indicators of Inflammation 36:12 The Importance of Urinary pH and Kidney Health 37:47 Root Causes of Obesity: Genetics, Environment, and Nutrient Deficiencies 39:14 The Impact of Prescription Drugs on Weight Gain 39:49 Magnesium Deficiency and Metabolic Syndrome 40:54 The Problem with Ultra-Processed Foods 42:36 The Importance of Personal Health Responsibility 44:11 Exploring Peptides and Their Benefits 48:54 Innovations in Longevity and Health Supplements 54:22 The Science Behind Synapsin and RG3 58:45 Conclusion and Final Thoughts   Dr. James Lavalle is an internationally recognized clinical pharmacist and a board certified clinical nutritionist for close to 40 years and he is the author of more than 20 books including, “Cracking the Metabolic Code.”  He has lectured for more than a decade for the American Academy of Anti-Aging Medicine.   Jim has served thousands of patients using his "Metabolic Model for Health" through his integrative health practice, LaValle Metabolix in Orange County, CA.   James is best known for his expertise in personalized integrative therapies uncovering the underlying metabolic issues that keep people from feeling healthy and vital.  His website is JimLavalle.com.  To find out more about his nutrition products that he has developed, including Synapsin, please go to MetabolicElite.co.   Dr. Ben Weitz is available for Functional Nutrition consultations specializing in Functional Gastrointestinal Disorders like IBS/SIBO and Reflux and also Cardiometabolic Risk Factors like elevated lipids, high blood sugar, and high blood pressure.  Dr. Weitz has also successfully helped many patients with managing their weight and improving their athletic performance, as well as sports chiropractic work by calling his Santa Monica office 310-395-3111.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.06.24.546170v1?rss=1 Authors: Stavsky, A., Parra-Rivas, L. A., Tal, S., Madhivanan, K., Roy, S., Gitler, D. Abstract: The cytosolic proteins synucleins and synapsins are thought to play cooperative roles in regulating synaptic vesicle (SV) recycling, but mechanistic insight is lacking. Here we identify the synapsin E-domain as an essential functional binding-partner of -synuclein (-syn). Synapsin E-domain allows -syn functionality, binds to -syn, and is necessary and sufficient for enabling effects of -syn at the synapse. Together with previous studies implicating the E-domain in clustering SVs, our experiments advocate a cooperative role for these two proteins in maintaining physiologic SV clusters. 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/2023.04.17.537179v1?rss=1 Authors: Stewart, A. N., Kumari, R., Bailey, W. M., Glaser, E. P., Hammers, G. V., Wireman, O. H., Gensel, J. C. Abstract: Restoring function in chronic stages of spinal cord injury (SCI) has often been met with failure or reduced efficacy when regenerative strategies are delayed past the acute or sub-acute stages of injury. Restoring function in the chronically injured spinal cord remains a critical challenge. We found that a single injection of retrogradely transported adeno-associated viruses (AAVrg) to knockout the phosphatase and tensin homolog protein (PTEN) in chronic SCI can effectively target both damaged and spared axons and restore locomotor functions in near-complete injury models. AAVrgs were injected to deliver cre recombinase and/or a red fluorescent protein (RFP) under the human Synapsin 1 promoter (hSyn1) into the spinal cords of C57BL/6 PTENFlox mice to knockout PTEN (PTEN-KO) in a severe thoracic SCI crush model at both acute and chronic time points. PTEN-KO improved locomotor abilities in both acute and chronic SCI conditions over a 9-week period. Regardless of whether treatment was initiated at the time of injury (acute), or three months after SCI (chronic), mice with limited hindlimb joint movement gained hindlimb weight support after treatment. Interestingly, functional improvements were not sustained beyond 9 weeks coincident with a loss of RFP reporter-gene expression and a near-complete loss of treatment-associated functional recovery by 6 months post-treatment. Treatment effects were also specific to severely injured mice; animals with weight support at the time of treatment lost function over a 6-month period. Retrograde tracing with Fluorogold revealed viable neurons throughout the motor cortex despite a loss of RFP expression at 9 weeks post-PTEN-KO. However, few Fluorogold labeled neurons were detected within the motor cortex at 6 months post-treatment. BDA labeling from the motor cortex revealed a dense corticospinal tract (CST) bundle in all groups except chronically treated PTEN-KO mice indicating a potential long-term toxic effect of PTEN-KO to neurons in the motor cortex. PTEN-KO mice had significantly more B-tubulin III labeled axons within the lesion when treatment was delivered acutely, but not chronically post-SCI. In conclusion, we have found that using AAVrgs to knockout PTEN is an effective manipulation capable of restoring motor functions in chronic SCI and can enhance axon growth of currently unidentified axon populations when delivered acutely after injury. However, the long-term consequences of PTEN-KO may exert neurotoxic effects. 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/2023.03.20.533583v1?rss=1 Authors: Song, S.-H., Augustine, G. J. Abstract: Synapsins cluster synaptic vesicles (SVs) to provide a reserve pool (RP) of SVs that maintains synaptic transmission during sustained activity. However, it is unknown how synapsins cluster SVs. Here we show that either liquid-liquid phase separation (LLPS) or tetramerization-dependent cross-linking can cluster SVs, depending upon whether a synapse is excitatory or inhibitory. Cell-free reconstitution revealed that both mechanisms can cluster SVs, with tetramerization bring more effective. At inhibitory synapses, perturbing synapsin-dependent LLPS impairs SV clustering and synchronization of GABA release, while perturbing synapsin tetramerization does not. At glutamatergic synapses, the opposite is true: synapsin tetramerization enhances clustering of glutamatergic SVs and mobilization of these SVs from the RP, while synapsin LLPS does not. Comparison of inhibitory and excitatory transmission during prolonged synaptic activity revealed that synapsin LLPS serves as a brake to limit GABA release, while synapsin tetramerization enables rapid mobilization of SVs from the RP to sustain glutamate release. 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/2023.01.11.523492v1?rss=1 Authors: Enders, J., Jack, J., Thomas, S., Lynch, P., Lasnier, S., Cao, X., Swanson, M. T., Ryals, J. M., Thyfault, J. P., Puchalska, P., Crawford, P. A., Wright, D. E. Abstract: Ketogenic diets are emerging as protective interventions in preclinical and clinical models of somatosensory nervous system disorders. Additionally, dysregulation of succinyl-CoA 3-oxoacid CoA-transferase 1 (SCOT, encoded by Oxct1), the fate-committing enzyme in mitochondrial ketolysis, has recently been described in Friedreich's ataxia and amyotrophic lateral sclerosis. However, the contribution of ketone metabolism in the normal development and function of the somatosensory nervous system remains poorly characterized. We generated sensory neuron-specific, Advillin-Cre knockout of Oxct1 (SNACKO) mice and characterized the structure and function of their somatosensory system. We used histological techniques to assess sensory neuronal populations, myelination, and innervation of the skin and spinal dorsal horn. We also examined cutaneous and proprioceptive sensory behaviors with the von Frey test, radiant heat assay, rotarod, and grid-walk tests. SNACKO mice exhibited myelination deficits, altered morphology of putative A{delta} soma from the dorsal root ganglion, reduced cutaneous innervation, and abnormal innervation of the spinal dorsal horn compared to wildtype mice. Synapsin 1-Cre-driven knockout of Oxct1 confirmed deficits in epidermal innervation following a loss of ketone oxidation. Loss of peripheral axonal ketolysis was further associated with proprioceptive deficits, yet SNACKO mice did not exhibit drastically altered cutaneous mechanical and thermal thresholds. Knockout of Oxct1 in peripheral sensory neurons resulted in histological abnormalities and severe proprioceptive deficits in mice. We conclude that ketone metabolism is essential for the development of the somatosensory nervous system. These findings also suggest that decreased ketone oxidation in the somatosensory nervous system may explain the neurological symptoms of Friedreich's ataxia. 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/2022.11.25.517123v1?rss=1 Authors: Gu, Y., Pope, A., Smith-Geater, C., Carmona, C., Johnstone, A., Shi, L., Chen, X., Santos, S., Bacon-Brenes, C. C., Shoff, T., Kleczko, K. M., Frydman, J., Thompson, L. M., Mobley, W. C., Wu, C. Abstract: Huntingtons disease (HD) results from a CAG repeat expansion in the gene for Huntington (HTT) resulting in expansion of the polyglutamine (Q) tract in the mutant protein (mHTT). Synaptic changes are early manifestations of neuronal dysfunction in HD. However, the mechanism(s) by which mHTT impacts synapse formation and function is not well defined. Herein we explored HD pathogenesis in the BACHD and the deltaN17-BACHD mouse models of HD by examining cortical synapse formation and function in primary cultures maintained for up to 35 days (DIV35). We identified synapses by immunostaining with antibodies against pre-synaptic (Synapsin 1) and a post-synaptic (PSD95) marker. Consistent with earlier studies, cortical neurons from both WT and the HD models began to form synapses at DIV14; at this age there were no genotypic differences in synapse numbers. However, from DIV21 through DIV35 BACHD neurons showed progressively smaller numbers of synapses relative to WT neurons. Remarkably, BACHD synaptic deficits were completely rescued by treating cultures with BDNF. Building on earlier studies using reagents inspired by the chaperonin TRiC, we found that addition of the recombinant apical domain of CCT1 partially rescued synapse number. Unexpectedly, unlike BACHD cultures, synapses in deltaN17-BACHD cultures showed a progressive increase in number as compared to WT neurons, thus distinguishing synaptic changes in these HD models. Using multielectrode arrays, we discovered age-related functional deficits in BACHD cortical cultures with significant differences present by DIV28. As for synapse number, BDNF treatment prevented most synaptic deficits, including mean firing rate, spikes per burst, inter-burst interval, and synchrony. The apical domain of CCT1 showed similar, albeit less potent effects. These data are evidence that deficits in HD synapse number and function can be replicated in vitro and that treatment with either BDNF or a TRiC-inspired reagent can prevent them. Our findings support the use of cellular models to further explicate HD pathogenesis and its treatments. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

In this episode of The Performance Medicine Show, Dr. Rogers answers YOUR health and wellness questions! What did you think of this episode of the podcast? Let us know by leaving a review! Connect with Performance Medicine! Sign up for our weekly newsletter: https://performancemedicine.net/doctors-note-sign-up/ Facebook: @PMedicine Instagram: @PerformancemedicineTN YouTube: Performance Medicine

You name it. We EXPLAIN it. In this episode of the podcast, Robin Riddle, NP-C explains how Synapsin is being used to help brain fog and promote cognitive health. What did you think of this episode of the podcast? Let us know by leaving a review! Connect with Performance Medicine! Sign up for our weekly newsletter: https://performancemedicine.net/doctors-note-sign-up/ Facebook: @PMedicine Instagram: @PerformancemedicineTN YouTube: Performance Medicine

Anxiety was escalating at a rapid rate before 2020, and now it's just crazy. Long-haulers, mandates, lockdowns, wars, masks, headlines, our kids.....let's just say it isn't expected to  get any better anytime soon, hence counseling services are increasing, doctors visits and prescriptions are increasing, but so are people searching for information and trying to solve their anxiety puzzle without medications, on their own. There are tons of options for medications, supplements, and general advice out there - where do you turn and what do you do?? Understand the mechanisms of anxiety, neuroinflammation, and autoimmunity. UNDERSTANDING MECHANISMS PROVIDE SOLUTIONS!I have at least 20 things in my Vitamin Store that I have used in my clinic that have helped people tremendously with anxiety, including magnesium, CBD, L-theanine, B6 and other B vitamins, keto diet, avoiding gluten or dairy, binders, methyl donors, sauna,  herbs for pathogens, probiotics, adaptogens, vagus nerve stimulation. Some of these people were mold, Lyme, EBV, IBS, or autoimmune disease patients with a list of 10+ other symptoms, but some were kids, moms, dads, people who just dealt with a lot of anxiety but otherwise had few complaints. It can happen to anybody. What are the mechanisms for YOU?? Here is a list of 10 things you need to know about when searching for the next clue to solve your health puzzle:1. Mitochondria - the batteries behind it all!! Also the cause behind it all.....listen to episodes 30, 31, 32 for more info on mitochondria but you have a QUADRILLION of them in your brain, so they are kinda important.....2. Brain Cells - Neurons vs. Microglia vs. Mast Cells vs. Astrocytes.....you don't need to know everything, but a little bit about each one can help!3. Brain Regions - limbic regions - amygdala, insula, hippocampus, hypothalamus; cerebellar-vestibular regions4. Neurotransmitters - GABA/Glutamate, Serotonin, Dopamine, Acetycholine, Epinephrine, Norepipheprine5. Hormones - HPA Axis (adrenals), Thyroid, Androgens, Estrogens, and most importantly Cortisol 6. Blood-Brain-Barrier - protector of the brain - damaged by head traumas, glutathione depletion, histamine, gut inflammation and permeability (leaky gut)7. Dysfunctional Pathways - Reactive Oxygen/Nitrogen Species (ROS/RNS), LPS, Mast Cell Activation, Kynurenine Pathway, Methylation, NO/ONOO, iNOS, excitotoxins (MSG, red 40), EMF radiation8. Nervous System Balance - Sympathetic/Parasympathetic balance - "fight or flight" vs. "rest and digest"9. Mitophagy/Autophagy - the clearing of "junk" from the brain10. Autoimmunity! - Self-tissue antibodies against things like GAD-65, cerebellum, thyroid, Myelin Basic Protein, Synapsin, Asiologanglioside, etcThese are 10 heavy topics!! But they are all important. You don't need to know everything about them, but knowing a little bit about each topic can help you figure out a bit more what's going on in your brain!

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.10.12.335778v1?rss=1 Authors: Bridi, J. C., Bereczki, E., Smith, S. K., Pocas, G. M., Kottler, B., Domingos, P., Elliott, C. J., Aarsland, D., Hirth, F. Abstract: Alpha-synuclein mislocalisation and accumulation in intracellular inclusions is the major pathological hallmark of degenerative synucleinopathies, including Parkinson's disease, Parkinson's disease with Dementia and Dementia with Lewy Bodies. Typical symptoms are behavioural abnormalities including motor deficits that mark disease progression, while non-motor symptoms and synaptic deficits are already apparent during the early stages of disease. Synucleinopathies have therefore been considered synaptopathies that exhibit synaptic dysfunction prior to neurodegeneration. However, the mechanisms and events underlying synaptopathy are largely unknown. Here we investigated the cascade of pathological events underlying alpha-synuclein accumulation and toxicity in a Drosophila model of synucleinopathy by employing a combination of histological, biochemical, behavioural and electrophysiological assays. Our findings demonstrate that targeted expression of human alpha-synuclein leads to its accumulation in presynaptic terminals that caused downregulation of synaptic proteins, Cysteine String Protein, Synapsin, and Syntaxin 1A, and a reduction in the number of Bruchpilot puncta, the core component of the presynaptic active zone essential for its structural integrity and function. These alpha-synuclein-mediated presynaptic alterations resulted in impaired neuronal function, which triggered behavioural deficits in ageing Drosophila that occurred prior to progressive degeneration of dopaminergic neurons. Comparable alterations in presynaptic active zone protein were found in patient brain samples of Dementia with Lewy Bodies. Together, these findings demonstrate that presynaptic accumulation of alpha-synuclein impairs the active zone and neuronal function, which together cause synaptopathy that results in behavioural deficits and the progressive loss of dopaminergic neurons. This sequence of events resembles the cytological and behavioural phenotypes that characterise the onset and progression of synucleinopathies, suggesting that alpha-synuclein mediated synaptopathy is an initiating cause of age-related neurodegeneration. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.24.220129v1?rss=1 Authors: Wang, S., Leem, J., Podvin, S., Hook, V., Kleschevnikov, N., Savchenko, P., Dhanani, M., Zhou, K., Kelly, I., Zhang, T., Miyanohara, A., Kleschevnikov, A., Wagner, S., Trojanowski, J., Roth, D., Patel, H., Patel, P., Head, B. P. Abstract: AD presents with severe neurodegeneration which leads to cognitive deficits and dementia. Identifying the molecular signals that attenuate neurodegeneration in AD may be exploited as therapeutic targets. This study revealed that transgenic AD mice (PSAPP) exhibit decreased caveolin-1 (Cav-1), a membrane/lipid raft (MLR) scaffolding protein that organizes synaptic signaling components. Subcellularly, Cav-1 and full length (fl)-TrkB were significantly decreased in MLRs. We thus developed an in vivo gene therapy that re-expresses neuronal-targeted Cav-1 using the synapsin promoter (SynCav1). While AD mice showed significant learning and memory deficits at 9 and 11 months, AD mice that received hippocampal SynCav1 (AD-SynCav1) maintained normal learning and memory at 9 and 11 months respectively. Furthermore, AD-SynCav1 mice showed preserved hippocampal MLR-localized fl-TrkB, synaptic ultrastructure, dendritic arborization and axonal myelin content, all of which occurred independent of reducing amyloid deposit and astrogliosis. Thus, SynCav1 demonstrates translational potential to treat AD by delaying neurodegeneration. Copy rights belong to original authors. Visit the link for more info

Cade and Regan Archibald discuss how we can enjoy our morning cup of joe without going overboard. The average American consumes three cups of coffee a day; this overstimulation means that they are more prone to stress and adrenal fatigue. Regan explains how coffee affects your adrenals and how much coffee you should consume, and when, to get the most out of your caffeine experience while still maintaining your health.   Key Takeaways: [2:45] Regan’s goal is to help make people more health-independent. [5:00] The bean roasting process can sometimes create cancerous agents. [5:40] How was coffee discovered? [8:10] Regan doesn’t recommend drinking three cups of coffee a day. Once your adrenals are healthy, he recommends a cup to a cup-and-a-half a day. [10:15] Do you need coffee to wake up in the morning? That’s not a good sign. Coffee should be looked at like medicine. [11:05] There are side effects if you consume too much coffee. [11:25] What do the effects of caffeine have on the human body? [15:25] Caffeine increases your cortisol, which will exhaust your adrenals over time. [17:45] Depending on how fast your metabolism is, Regan recommends at what time of the day you should stop drinking coffee. [20:15] Did you know you can get some caffeine in your system just by smelling coffee? [22:50] What is a nootropic? [25:00] Cade has experienced better mental clarity when he uses nootropics. [27:25] What is Semax? [33:50] What is Selank? [39:20] What is RG3 synapsin? [48:05] Remember, caffeine and coffee is a medicine.   Mentioned in This Episode: Go Wellness website: Go Wellness Call Regan: 801-582-2011 Email Regan: regan@gowellness.com Email the Team: info@gowellness.com or EastWestAcu@Gmail.com Clinic: Acueastwest.com Yourhealthyself.com Getkion.com Semax nootropic Selank nootropic Synapsin

Ray talks about rG3/Synapsin nasal spray and what symptoms it can help with.

Ray talks about brain fog, dementia, synapsin and memory.

Two pharmacists! Pharmacist and Certified Clinical Nutritionist (CCN), Ray Solano of PDLabs will help us understand how the increase in allergies, GERD, constipation and autoimmune diseases (think rheumatoid arthritis and lupus for example) are connected to a new class of drugs (think Humara). Their other side effects include leukemia and blood disorders. Joining him is  Jim LaValle, a pharmacist, CCN and prolific author. He wrote Your Blood Never Lies: How to Read a Blood Test for a Longer, Healthier Life, and the bestseller, Cracking the Metabolic Code: 9 Keys to Optimal Health. We also discussed the brain product Synapsin. Then Dr. Ross Pelton R.Ph., Ph.D., CCN will talk about summer digestive issues. He is the Scientific Director for Essential Formulas, Inc.  At the end of the show we will talk with Charlotte Yorkson of Kaleidoscope Farm about a wonderfully natural way to fertilize all of our plants.  

Two pharmacists! Pharmacist and Certified Clinical Nutritionist (CCN), Ray Solano of PDLabs will help us understand how the increase in allergies, GERD, constipation and autoimmune diseases (think rheumatoid arthritis and lupus for example) are connected to a new class of drugs (think Humara). Their other side effects include leukemia and blood disorders. Joining him is  Jim LaValle, a pharmacist, CCN and prolific author. He wrote Your Blood Never Lies: How to Read a Blood Test for a Longer, Healthier Life, and the bestseller, Cracking the Metabolic Code: 9 Keys to Optimal Health. We also discussed the brain product Synapsin. Then Dr. Ross Pelton R.Ph., Ph.D., CCN will talk about summer digestive issues. He is the Scientific Director for Essential Formulas, Inc.  At the end of the show we will talk with Charlotte Yorkson of Kaleidoscope Farm about a wonderfully natural way to fertilize all of our plants.  

Ray's Healthy Tidbit About Synapsin, Memory Issues & Prescription Drugs Episode 072 by Ray Solano

Why You Should Listen: In this episode, you will learn the factors involved in dementia and Alzheimer's and potential solutions discussed in "The End of Alzheimer's". About My Guest: My guest for this episode is Dr. Dale Bredesen.  Dale Bredesen, MD is internationally recognized as an expert in the mechanisms of neurodegenerative diseases such as Alzheimer’s disease. He graduated from Caltech, then earned his MD from Duke University Medical Center in Durham, NC. He served as Chief Resident in Neurology at the University of California, San Francisco (UCSF) before joining Nobel laureate Stanley Prusiner’s laboratory at UCSF as an NIH Postdoctoral Fellow. He held faculty positions at UCSF, UCLA and the University of California, San Diego. Dr. Bredesen directed the Program on Aging at the Burnham Institute before coming to the Buck Institute in 1998 as its founding President and CEO. The uniform failure of recent drug trials in Alzheimer’s disease has highlighted the critical need for a more accurate understanding of the fundamental nature of Alzheimer’s disease. Dr. Bredesen’s research has led to new insights that explain the erosion of memory seen in Alzheimer’s disease, and these insights have opened the door to a new therapeutic approach. His book "The End of Alzheimer's: The First Program to Prevent and Reverse Cognitive Decline" was released just over a year ago and is a hopeful exploration into not only the condition, but to solutions that are helping people with Alzheimer's improve their quality of life today. Key Takeaways: - How big of a problem is Alzheimer's? - What is the role of apoE in the potential for Alzheimer's development? - What are the primary risk factors for the development of Alzheimer's? - Why is amyloid a potentially a good thing and not something to focus on removing without first addressing underlying causes? - What are the subtypes of Alzheimer's? - How does insulin sensitivity play a role om Alzheimer's? - What factors play a role in the the "Toxic" subtype 3? - What is the role of Lyme disease and mold illness in the development of Alzheimer's? - What is a "Cognoscopy" and how is it performed? - What is the "ReCode" protocol and how is treatment approached? - How are VIP and Synapsin potentially helpful in reversing cognitive decline? - Does Mast Cell Activation Syndrome play a role in the inflammation associated with Alzheimer's? - Is detoxification important in recovering cognitive function? - Which binders are helpful in supporting detoxification? - Does EMF exposure play a role in the development of Alzheimer's? Connect With My Guest: https://ApolloHealthCo.com Interview Date: January 16, 2019 Additional Information: To learn more, visit http://BetterHealthGuy.com. Disclaimer: The content of this show is for informational purposes only and is not intended to diagnose, treat, or cure any illness or medical condition. Nothing in today's discussion is meant to serve as medical advice or as information to facilitate self-treatment. As always, please discuss any potential health-related decisions with your own personal medical authority.

Dr. Jim Lavalle and host, Ray Solano talk about RG3/Synapsin and how it can help when your body is stressed.

Dr. Jim Lavalle and host, Ray Solano talk about RG3/Synapsin and how it can help when your body is stressed. Ray also talks about PD Labs Winter Immune Kit that will help you this flu season

Why You Should Listen: In this episode, you will learn about mold illness, Chronic Inflammatory Response Syndrome (CIRS), and "Life After Mold". About My Guest: My guest for this episode is Dr. Lauren Tessier. Lauren Tessier, ND is a Naturopathic Physician licensed in the state of Vermont. She received her Bachelors in Premedical Sciences and Health Psychology from Massachusetts College of Pharmacy in Boston and later became a Naturopathic Physician at Bastyr University in Kenmore, Washington. Her practice, Life After Mold, uses a patient-centered approach to help recover those that are suffering from mold-related illness. She combines naturopathic, functional, and integrative medicine to address the entire person. She is a Shoemaker Certified Physician specializing in the treatment of Chronic Inflammatory Response Syndrome (CIRS) which results from exposure to water-damaged buildings. In 2011, Hurricane Irene created an unimaginable flood in Waterbury, Vermont, and she was unprepared for what she would see next in her practice. Patients were ill with unexplained rashes, allergies that did not respond to treatment, fatigue, breathing difficulties, neurological complaints, headaches, nausea, and immune system dysfunction. When her normal approaches no longer worked for these patients, she dove deep into mold-related illness. Her practice is dedicated to helping those suffering with mold, biotoxin, and mycotoxin associated illness resulting from water-damaged buildings. As time passed, she came to the belief that the environment plays a role in all chronic illness. Environmental illness includes mold, heavy metals, glyphosate exposure, chronic infections such as Lyme disease, Multiple Chemical Sensitivity, and Mast Cell Activation Syndrome. Dr. Tessier is an Executive Board Member of the International Society for Environmentally Acquired Illness (ISEAI) which aims to advance medical knowledge surrounding environmentally acquired illness. Key Takeaways: - What are some of the environmental factors that may predispose an environment to water-damage and the potential for mold illness? - What are some of the illness-creating substances that are found in a water-damaged building? - What are common symptoms of CIRS? - Are there basic screening tests that can be performed of an environment before investing in an IEP? - How important are the HLA haplotypes in CIRS? - Is there clinical value in urinary mycotoxin testing? - Can molds encountered in a water-damaged building lead to colonization within the body? - When considering binders, what is absorption vs. adsorbtion? - Why is bile flow important and how might it be supported? - What options might help reducing inflammation in those with CIRS? - Are there downsides of exogenous glutathione supplementation? - How important is eradicating MARCoNS in CIRS? - How might VIP and Synapsin be helpful in those with CIRS? - What triggers Mast Cell Activation Syndrome (MCAS) and how might it be addressed? - When someone feels significantly worse, what rescue items might help to move through a detox or Herxheimer reaction? - Is there a role for limbic system retraining in CIRS? Connect With My Guest: http://lifeaftermold.com Interview Date: September 28, 2018 Additional Information: To learn more, visit http://BetterHealthGuy.com. Disclaimer: The content of this show is for informational purposes only and is not intended to diagnose, treat, or cure any illness or medical condition. Nothing in today's discussion is meant to serve as medical advice or as information to facilitate self-treatment. As always, please discuss any potential health-related decisions with your own personal medical authority.

Chronic stress involves a response to emotional pressure experienced for a long period of time. It is also a source of depressive disorders. Recent studies have suggested that chronic stress does not only have mental impacts, but also molecular impacts, specifically on cognition. In this study, it is hypothesized that chronic stress does have an influence on cognitive function. From hippocampal samples of repeated social defeat stressed mice and control mice, both mRNA levels and protein levels were analyzed. RNA was isolated, reverse transcribed, and a real-time quantitative PCR was conducted. For the proteins, after isolation, a BCA protein assay was conducted, and then multiple western blots were performed to observe their expression. Afterwards, data were collected and analyzed. A student’s t-test was performed to determine the significance of any change observed in the stressed mice. BDNF V, Synapsin 1 and Synapsin 2, at the mRNA level, were found to be significantly downregulated. At the protein level, pCREB was found to be surprisingly upregulated in the stressed mice. Overall, this chronic stress does impact cognition, but only to a certain extent and in variation.

Take control of your healthy with Dr. James LaValle author of “Your Blood Never Lies” and founder of the Synapsin nasal spray joins host Ray Solano for clinical pearls found in a simple blood tests that may improve your health.