Podcasts about alzheimer's disease ad

CME credits: 1.25 Valid until: 31-01-2025 Claim your CME credit at https://reachmd.com/programs/cme/is-amyloid-targeting-therapy-worth-it/16466/ Alzheimer's Disease (AD) has historically been a condition associated with more questions than answers. These questions are only increasing with the flurry of developmental activity in recent years, particularly the introduction of the first ever disease modifying therapies, as the clinical picture is dramatically changing each day. To help address rising challenges prompted by this shifting paradigm, this activity features real questions from practicing clinicians regarding the integration of and expert perspectives on amyloid-targeting therapies for the treatment of AD. Note: This program was recorded prior to the January 31, 2024 decision to withdraw aducanumab from the market. Though amyloid targeting therapy is available, this particular agent can no longer be prescribed. For more information, see: https://investors.biogen.com/news-releases/news-release-details/biogen-realign-resources-alzheimers-disease-franchise

CME credits: 1.25 Valid until: 31-01-2025 Claim your CME credit at https://reachmd.com/programs/cme/do-women-respond-differently-to-att-than-men/16344/ Alzheimer's Disease (AD) has historically been a condition associated with more questions than answers. These questions are only increasing with the flurry of developmental activity in recent years, particularly the introduction of the first ever disease modifying therapies, as the clinical picture is dramatically changing each day. To help address rising challenges prompted by this shifting paradigm, this activity features real questions from practicing clinicians regarding the integration of and expert perspectives on amyloid-targeting therapies for the treatment of AD. Note: This program was recorded prior to the January 31, 2024 decision to withdraw aducanumab from the market. Though amyloid targeting therapy is available, this particular agent can no longer be prescribed. For more information, see: https://investors.biogen.com/news-releases/news-release-details/biogen-realign-resources-alzheimers-disease-franchise

CME credits: 1.25 Valid until: 31-01-2025 Claim your CME credit at https://reachmd.com/programs/cme/what-types-of-changes-if-any-should-we-expect-with-amyloid-targeting-therapy/16343/ Alzheimer's Disease (AD) has historically been a condition associated with more questions than answers. These questions are only increasing with the flurry of developmental activity in recent years, particularly the introduction of the first ever disease modifying therapies, as the clinical picture is dramatically changing each day. To help address rising challenges prompted by this shifting paradigm, this activity features real questions from practicing clinicians regarding the integration of and expert perspectives on amyloid-targeting therapies for the treatment of AD. Note: This program was recorded prior to the January 31, 2024 decision to withdraw aducanumab from the market. Though amyloid targeting therapy is available, this particular agent can no longer be prescribed. For more information, see: https://investors.biogen.com/news-releases/news-release-details/biogen-realign-resources-alzheimers-disease-franchise

CME credits: 1.25 Valid until: 31-01-2025 Claim your CME credit at https://reachmd.com/programs/cme/what-does-aria-look-like-clinically/16342/ Alzheimer's Disease (AD) has historically been a condition associated with more questions than answers. These questions are only increasing with the flurry of developmental activity in recent years, particularly the introduction of the first ever disease modifying therapies, as the clinical picture is dramatically changing each day. To help address rising challenges prompted by this shifting paradigm, this activity features real questions from practicing clinicians regarding the integration of and expert perspectives on amyloid-targeting therapies for the treatment of AD. Note: This program was recorded prior to the January 31, 2024 decision to withdraw aducanumab from the market. Though amyloid targeting therapy is available, this particular agent can no longer be prescribed. For more information, see: https://investors.biogen.com/news-releases/news-release-details/biogen-realign-resources-alzheimers-disease-franchise

CME credits: 1.25 Valid until: 31-01-2025 Claim your CME credit at https://reachmd.com/programs/cme/how-should-we-monitor-patients-on-amyloid-targeting-therapy/16341/ Alzheimer's Disease (AD) has historically been a condition associated with more questions than answers. These questions are only increasing with the flurry of developmental activity in recent years, particularly the introduction of the first ever disease modifying therapies, as the clinical picture is dramatically changing each day. To help address rising challenges prompted by this shifting paradigm, this activity features real questions from practicing clinicians regarding the integration of and expert perspectives on amyloid-targeting therapies for the treatment of AD. Note: This program was recorded prior to the January 31, 2024 decision to withdraw aducanumab from the market. Though amyloid targeting therapy is available, this particular agent can no longer be prescribed. For more information, see: https://investors.biogen.com/news-releases/news-release-details/biogen-realign-resources-alzheimers-disease-franchise

CME credits: 1.25 Valid until: 31-01-2025 Claim your CME credit at https://reachmd.com/programs/cme/how-do-you-counsel-patients-about-amyloid-related-imaging-abnormalities/16340/ Alzheimer's Disease (AD) has historically been a condition associated with more questions than answers. These questions are only increasing with the flurry of developmental activity in recent years, particularly the introduction of the first ever disease modifying therapies, as the clinical picture is dramatically changing each day. To help address rising challenges prompted by this shifting paradigm, this activity features real questions from practicing clinicians regarding the integration of and expert perspectives on amyloid-targeting therapies for the treatment of AD. Note: This program was recorded prior to the January 31, 2024 decision to withdraw aducanumab from the market. Though amyloid targeting therapy is available, this particular agent can no longer be prescribed. For more information, see: https://investors.biogen.com/news-releases/news-release-details/biogen-realign-resources-alzheimers-disease-franchise

CME credits: 1.25 Valid until: 31-01-2025 Claim your CME credit at https://reachmd.com/programs/cme/how-much-should-we-worry-about-amyloid-related-imaging-abnormalities/16339/ Alzheimer's Disease (AD) has historically been a condition associated with more questions than answers. These questions are only increasing with the flurry of developmental activity in recent years, particularly the introduction of the first ever disease modifying therapies, as the clinical picture is dramatically changing each day. To help address rising challenges prompted by this shifting paradigm, this activity features real questions from practicing clinicians regarding the integration of and expert perspectives on amyloid-targeting therapies for the treatment of AD. Note: This program was recorded prior to the January 31, 2024 decision to withdraw aducanumab from the market. Though amyloid targeting therapy is available, this particular agent can no longer be prescribed. For more information, see: https://investors.biogen.com/news-releases/news-release-details/biogen-realign-resources-alzheimers-disease-franchise

CME credits: 1.25 Valid until: 31-01-2025 Claim your CME credit at https://reachmd.com/programs/cme/which-biomarkers-do-you-recommend-to-confirm-amyloid-positivity/16338/ Alzheimer's Disease (AD) has historically been a condition associated with more questions than answers. These questions are only increasing with the flurry of developmental activity in recent years, particularly the introduction of the first ever disease modifying therapies, as the clinical picture is dramatically changing each day. To help address rising challenges prompted by this shifting paradigm, this activity features real questions from practicing clinicians regarding the integration of and expert perspectives on amyloid-targeting therapies for the treatment of AD. Note: This program was recorded prior to the January 31, 2024 decision to withdraw aducanumab from the market. Though amyloid targeting therapy is available, this particular agent can no longer be prescribed. For more information, see: https://investors.biogen.com/news-releases/news-release-details/biogen-realign-resources-alzheimers-disease-franchise

CME credits: 1.25 Valid until: 31-01-2025 Claim your CME credit at https://reachmd.com/programs/cme/what-is-the-role-of-apoe4-testing-in-alzheimers-disease/16337/ Alzheimer's Disease (AD) has historically been a condition associated with more questions than answers. These questions are only increasing with the flurry of developmental activity in recent years, particularly the introduction of the first ever disease modifying therapies, as the clinical picture is dramatically changing each day. To help address rising challenges prompted by this shifting paradigm, this activity features real questions from practicing clinicians regarding the integration of and expert perspectives on amyloid-targeting therapies for the treatment of AD. Note: This program was recorded prior to the January 31, 2024 decision to withdraw aducanumab from the market. Though amyloid targeting therapy is available, this particular agent can no longer be prescribed. For more information, see: https://investors.biogen.com/news-releases/news-release-details/biogen-realign-resources-alzheimers-disease-franchise

CME credits: 1.25 Valid until: 31-01-2025 Claim your CME credit at https://reachmd.com/programs/cme/whats-the-best-way-to-identify-mild-cognitive-impairment-and-early-alzheimers-disease/16336/ Alzheimer's Disease (AD) has historically been a condition associated with more questions than answers. These questions are only increasing with the flurry of developmental activity in recent years, particularly the introduction of the first ever disease modifying therapies, as the clinical picture is dramatically changing each day. To help address rising challenges prompted by this shifting paradigm, this activity features real questions from practicing clinicians regarding the integration of and expert perspectives on amyloid-targeting therapies for the treatment of AD. Note: This program was recorded prior to the January 31, 2024 decision to withdraw aducanumab from the market. Though amyloid targeting therapy is available, this particular agent can no longer be prescribed. For more information, see: https://investors.biogen.com/news-releases/news-release-details/biogen-realign-resources-alzheimers-disease-franchise

CME credits: 1.25 Valid until: 31-01-2025 Claim your CME credit at https://reachmd.com/programs/cme/which-amyloid-targeting-therapy-is-best/16335/ Alzheimer's Disease (AD) has historically been a condition associated with more questions than answers. These questions are only increasing with the flurry of developmental activity in recent years, particularly the introduction of the first ever disease modifying therapies, as the clinical picture is dramatically changing each day. To help address rising challenges prompted by this shifting paradigm, this activity features real questions from practicing clinicians regarding the integration of and expert perspectives on amyloid-targeting therapies for the treatment of AD. Note: This program was recorded prior to the January 31, 2024 decision to withdraw aducanumab from the market. Though amyloid targeting therapy is available, this particular agent can no longer be prescribed. For more information, see: https://investors.biogen.com/news-releases/news-release-details/biogen-realign-resources-alzheimers-disease-franchise

CME credits: 1.25 Valid until: 31-01-2025 Claim your CME credit at https://reachmd.com/programs/cme/what-are-the-data-behind-att/16334/ Alzheimer's Disease (AD) has historically been a condition associated with more questions than answers. These questions are only increasing with the flurry of developmental activity in recent years, particularly the introduction of the first ever disease modifying therapies, as the clinical picture is dramatically changing each day. To help address rising challenges prompted by this shifting paradigm, this activity features real questions from practicing clinicians regarding the integration of and expert perspectives on amyloid-targeting therapies for the treatment of AD. Note: This program was recorded prior to the January 31, 2024 decision to withdraw aducanumab from the market. Though amyloid targeting therapy is available, this particular agent can no longer be prescribed. For more information, see: https://investors.biogen.com/news-releases/news-release-details/biogen-realign-resources-alzheimers-disease-franchise

Research at Boston University has led to the discovery of a non-invasive method to diagnose Alzheimer's.  This opens the door in the coming years to possibly detecting the disease in its early stages, decades before real symptoms appear.  Manju Subramanian, MD and her team found that proteins in eye fluids are providing this window to the brain. These eye fluids are confirming pathological brain conditions like dementia in the Alzheimer's form. Until now, MRIs and lumbar punctures were the tools to aid the clinical diagnosis of Alzheimer's, but that has meant late detection when the disease is already in place. Alzheimer's is not actually confirmed until after death and a post-mortem examination of the brain is done.  "We know that patients with eye disease tend to be an at-risk population for dementia. Patients with macular degeneration, glaucoma and diabetic retinopathy, those are the three big ones," says Subramanian. The potential of an eye fluid exam at an optometrist's office is ideal as it's non-invasive and not expensive.  But, it is still several years out before potentially becoming commonplace.  More research is needed. Still to be determined in future research is just how early eye fluid proteins become abnormal when dementia is developing.   "As they say, the eye is the window to the soul.  It is also very much the window to the brain," says Subramanian. ***** Manju Subramanian is an Associate Professor in Ophthalmology and Vice-Chairman of Faculty Affairs. She is an ophthalmic surgeon specializing in Vitreoretinal Disease and Surgery, and is in academic practice at Boston Medical Center. She also sees patients at the Dedham Ophthalmic Consultants. Her primary areas of clinical interest include medical and surgical management of diabetic retinopathy, age-related macular degeneration, retinal detachments, hereditary retinal diseases, ocular inflammation, and ocular trauma. Dr. Subramanian graduated from the University of Missouri School of Medicine and completed her residency at the University of Kansas Medical Center in 2002. She completed a fellowship in Vitreoretinal Disease and Surgery at Tufts University School of Medicine and Ophthalmic Consultants of Boston in 2004. Dr. Subramanian's research interests include the study of eye-based biomarkers for Alzheimer's Disease (AD), age-related macular degeneration, diabetic retinopathy, and the role of anesthesia in eye surgery. She was Principal Investigator for the first head to head clinical trial comparing the use of bevacizumab and ranibizumab in the treatment of age-related macular degeneration, and she is currently the Principal Investigator for a study assessing the role of oral sedation in eye surgery. She is also a recent recipient of an R03 Grant Award by the National Institutes of Aging as the Principal Investigator of a study looking at protein biomarkers for AD in the eye. In her role as Vice-Chairman of Faculty Affairs at Boston University Eye Associates, she works in a supportive role in the professional and career development and engagement of the clinical faculty. Prior to 2017, she served as the Vice-Chairman of Clinical Services for 8 years. She serves on several institutional committees, including the Women's Leadership Advisory Council, the Boston University Medical Group (BUMG) Research Committee, the BU School of Medicine Promotion Criteria Working Group, and also serves as Chair of the BUMG Professional Development Committee. She additionally serves on national committees, such as the International Meetings Committee for the American Academy of Ophthalmology (AAO), the Diversity Initiatives Committee for the Association for Research in Vision and Ophthalmology (ARVO), and a Special Emphasis Panel for a Study Section with the National Institutes of Health. ***** Cutting Edge Health podcast website: https://cuttingedgehealth.com/ Cutting Edge Health Social and YouTube: YouTube channel: youtube.com/@cuttingedgehealthpodcast Instagram - https://instagram.com/cuttingedgehealthpodcast Facebook - https://www.facebook.com/Cutting-Edge-Health-Podcast-with-Jane-Rogers-101036902255756 Please note that the information provided in this show is not medical advice, nor should it be taken or applied as a replacement for medical advice. The Cutting Edge Health podcast, its employees, guests and affiliates assume no liability for the application of the information discussed. Special thanks to Alan, Maria, Louis, and Nicole on the Cutting Edge Health team!

CME credits: 0.50 Valid until: 24-08-2024 Claim your CME credit at https://reachmd.com/programs/cme/understanding-the-fine-print-the-who-when-and-what-to-do-about-aria-in-patients-with-alzheimers-disease-radiology-module/14852/ Recently, Alzheimer's Disease (AD) saw its first approvals for disease modifying therapy (DMT). With amyloid-beta (Aβ) targeting DMT now a reality, the entire way this condition is viewed and managed is changing. In particular, amyloid-related imaging abnormalities (ARIA), the most common adverse effects seen in DMT trials, are unique to this agent class, raising new questions and considerations across multiple medical specialties. As there is limited formal guidance on how to recognize and mange ARIA, this program employs experts in the fields of neurology, radiology, emergency medicine, and primary care to provide insight into how their fields are evolving to accommodate ARIA and to outline individual roles and best practices across specialties. This activity is part of a series of six distinct programs designed to introduce ARIA, detail its recognition and management in specific clinical settings, and ultimately optimize collaborative care. This activity focuses on the role of radiologists in the risk stratification, recognition, and management of ARIA. Note that the core activity is supplemented by an interactive clinical summary designed specifically for radiologists. This convenient, mobile-friendly tool was developed to assist clinicians in considering how best to implement ARIA guidelines into their …=

CME credits: 0.50 Valid until: 26-07-2024 Claim your CME credit at https://reachmd.com/programs/cme/understanding-the-fine-print-the-who-when-and-what-to-do-about-aria-in-patients-with-alzheimers-disease-neurology-module/14849/ Recently, Alzheimer's Disease (AD) saw its first approvals for disease modifying therapy (DMT). With amyloid-beta (Aβ) targeting DMT now a reality, the entire way this condition is viewed and managed is changing. In particular, amyloid-related imaging abnormalities (ARIA), the most common adverse effects seen in DMT trials, are unique to this agent class, raising new questions and considerations across multiple medical specialties. As there is limited formal guidance on how to recognize and mange ARIA, this program employs experts in the fields of neurology, radiology, emergency medicine, and primary care to provide insight into how their fields are evolving to accommodate ARIA and to outline individual roles and best practices across specialties. This activity is part of a series of six distinct programs designed to introduce ARIA, detail its recognition and management in specific clinical settings, and ultimately optimize collaborative care. This activity focuses on the role of neurology clinicians including when to raise clinical suspicion of ARIA in the clinic, how to evaluate suspected ARIA, and what courses of action may be needed to treat/manage ARIA should it occur. Note that the core activity is supplemented by an interactive clinical summary …=

CME credits: 0.50 Valid until: 26-06-2024 Claim your CME credit at https://reachmd.com/programs/cme/understanding-the-fine-print-the-who-when-and-what-to-do-about-aria-in-patients-with-alzheimers-disease-emergency-medicine-module/14851/ Recently, Alzheimer's Disease (AD) saw its first approvals for disease modifying therapy (DMT). With amyloid-beta (Aβ) targeting DMT now a reality, the entire way this condition is viewed and managed is changing. In particular, amyloid-related imaging abnormalities (ARIA), the most common adverse effects seen in DMT trials, are unique to this agent class, raising new questions and considerations across multiple medical specialties. As there is limited formal guidance on how to recognize and mange ARIA, this activity series employs experts in the fields of neurology, radiology, emergency medicine, and primary care to provide insight into how their fields are evolving to accommodate ARIA and to outline individual roles and best practices across specialties. This activity is part of a series of six distinct programs designed to introduce ARIA, detail its recognition and management in specific clinical settings, and ultimately optimize collaborative care. This activity focuses on the role of emergency medicine clinicians in the recognition and management of ARIA. This includes an overview of how ARIA may present to the emergency department and what courses of action to treat/manage ARIA may be needed from the hospital care team. Note that the core activity is supplemented by an

CME credits: 0.50 Valid until: 26-06-2024 Claim your CME credit at https://reachmd.com/programs/cme/understanding-the-fine-print-the-who-when-and-what-to-do-about-aria-in-patients-with-alzheimers-disease-closing-module/14853/ Recently, Alzheimer's Disease (AD) saw its first approvals for disease modifying therapy (DMT). With amyloid-beta (Aβ) targeting DMT now a reality, the entire way this condition is viewed and managed is changing. In particular, amyloid-related imaging abnormalities (ARIA), the most common adverse effects seen in DMT trials, are unique to this agent class, raising new questions and considerations across multiple medical specialties. As there is limited formal guidance on how to recognize and mange ARIA, this activity series employs experts in the fields of neurology, radiology, emergency medicine, and primary care to provide insight into how their fields are evolving to accommodate ARIA and to outline individual roles and best practices across specialties. This activity is part of a series of six distinct programs designed to introduce ARIA, detail its recognition and management in specific clinical settings, and ultimately optimize collaborative care. This activity finishes out the series by first providing an abbreviated outline of what has been addressed across activities 1-5 followed by a multidisciplinary discussion of questions and considerations that may impact the team-based execution of discussed strategies. =

CME credits: 0.50 Valid until: 15-05-2024 Claim your CME credit at https://reachmd.com/programs/cme/understanding-the-fine-print-the-who-when-and-what-to-do-about-aria-in-patients-with-alzheimers-disease/14848/ Recently, Alzheimer's Disease (AD) saw its first approvals for disease-modifying therapy (DMT). With amyloid-beta (Aβ) targeting DMT now a reality, the entire way this condition is viewed and managed is changing. In particular, amyloid-related imaging abnormalities (ARIA), the most common adverse effects seen in DMT trials, are unique to this agent class, raising new questions and considerations across multiple medical specialties. As there is limited formal guidance on how to recognize and mange ARIA, this activity series employs experts in the fields of neurology, radiology, emergency medicine, and primary care to provide insight into how their fields are evolving to accommodate ARIA and to outline individual roles and best practices across specialties. This six-part series features distinct programs designed to introduce ARIA, detail its recognition and management in specific clinical settings, and ultimately optimize collaborative care. This first activity focuses on the rise of amyloid-targeting DMT and the subsequent key features of ARIA that impact all specialties. =

Laynie Dratch of Penn Medicine comes onto the podcast to answer all of our burning questions about working with a genetic counselor. We loved chatting with her so much that we may need to follow up with a part 2! Let us know what other questions you have for Laynie on our episode art on instagram @remembermepodcast. A list of resources mentioned in this episode are all linked here on our blog. Laynie Dratch, ScM, CGC is a genetic counselor in adult neurology at the University of Pennsylvania in Philadelphia, PA, specializing in Frontotemporal Degeneration (FTD) spectrum disorders.  She helps families with adult-onset conditions such as FTD, Amyotrophic Lateral Sclerosis (ALS), Alzheimer's Disease (AD), and others, navigate genetic testing options and cope with their diagnoses through research and clinical encounters. Her research interests include the lived experiences of individuals with or at risk of developing FTD, issues in predictive genetic testing, and genetic counseling access and service delivery. She is a co-founder of the annual Penn Familial FTD/ALS Conference, as well as the co-founder and chair of the ALS/FTD Working Group within the National Society of Genetic Counselors. Laynie graduated summa cum laude from Colgate University with a BA in neuroscience and a minor in psychology. She completed her master's in genetic counseling at the Johns Hopkins University and the National Institutes of Health. --- Thank you to our sponsor of this episode and Season 7, ⁠⁠LearnFTD⁠⁠. LearnFTD is working to raise awareness of gene mutations in FTD and the importance of genetic testing. Visit ⁠⁠LearnFTD.com⁠⁠ for information and resources on FTD, genetics, and a video providing an overview of genetic testing and counseling. You can also follow LearnFTD on ⁠⁠Facebook⁠⁠ and ⁠⁠Instagram⁠⁠ @LearnFTD. --- ⁠⁠Remember Me⁠⁠ is a podcast created by two moms who became fast friends on Instagram while caregiving for their parents. It features stories of Frontotemporal Dementia - FTD - with a focus on remembering individuals for who they were before the disease. The stories shared are raw, real, and so full of love. We hope it inspires you to "accept the good." "Always, always, accept the good." --- Support this podcast: https://podcasters.spotify.com/pod/show/rememberme/support

Think after 40 muscle is a thing of the past? Think again!  There was a time when I was a cardio bunny. I dabbled in strength training but spent hours each week, sometimes a day, doing “aerobics.”  We tend to think, because we were told it so often for decades, that aerobic activity is best for fitness. Even though more and more science featuring postmenopausal women shows muscle has the most influence on numerous components of health, we're still drawn to “cardio.”  Are you at a point what you're doing isn't working, yet found yourself reluctant to exchange cardio for strength training? This is for you.  Women Need Muscle-Centric Exercise More Than Men Women begin with less muscle and more fat than men. Fat is essential for reproduction. Once hormones needed for reproduction, but also muscle maintenance, decline during the menopause transition, fat tends to increase and muscle loss is pronounced.  One reason that “cardio” doesn't “burn the fat” or boost metabolism is that with the decline of sex hormones, women are more susceptible to negative effects of stress. (2) Cardio, in the way we've always done it, tends to increase stress. (3) At this same time, women tend to become more insulin resistant. A body under stress stores fat in a form of self-preservation. It can't both burn and store fat. The stress hormone cortisol and insulin team up and tend to increase fat deposits around the belly. At midlife, doing more cardio to lose belly weight may actually cause more belly fat.  Keep Stress Low Short walks, even longer hikes, or short bursts of high intensity can certainly reduce the overall stress impact of exercise. That is, keep the stress positive. That hinges most on whether you enjoy, or find joy in, the activity and monitor your stress from all areas of life, adjusting as needed. However, these cardio activities don't influence fat burning beyond the activity. They don't increase muscle mass. Exercise that increases lean muscle mass, however, will not only improve body composition, but many of the symptoms of menopause, and increases healthy lifespan. This goes far beyond just risk of falls.  After 40 muscle is harder, not impossible to build. After 50 it's harder than that. Start.  You've Been Robbed Muscle loss begins at about 30. Studies vary on rate of loss being approximately 3-8% per decade or up to 1% annually after 30 but agree this rate is even higher both during the menopause transition and increases after 60. In severe instances, there is 50% total muscle loss by 80.   Muscle mass losses alter body composition (less muscle means more fat even if you don't gain fat) and are directly correlated with insulin resistance. Not only is this acutely frustrating for women with stubborn weight or belly fat, but long term can lead to type 2 diabetes, obesity, heart disease and osteoporosis.  Recent History's Influence on Muscle and Health Though we're past the worst of the pandemic, we're going to see consequences of the pandemic for years. On average 42% of the population gained weight, on average 29 lbs., during the pandemic.  It wasn't muscle. Gyms were closed. Dumbbells weren't available. For women during the menopause transition when muscle and bone loss can accelerate significantly, (8) is greater chance of early disability. Lack of the muscle stimulus from estrogen combined with lack of strength training to offset it, could mean greater levels of sarcopenia and osteoporosis if not mitigated. Basic Muscle Facts  To gain muscle, you need strength, or resistance training. Women need strength training more than cardio. Women need strength training even more than men. Women 50 or older need strength training more than women 30.  Menopause-Related Reasons to Gain Muscle in Midlife Let's be honest, we're more motivated by immediate gratification than long term risk aversion. Muscle provides both. Well-documented menopause symptoms include but are not limited to: Insomnia Depression Anxiety Hot Flashes  Night Sweats  Weight Gain Fat gain Loss of muscle tone Belly Fat Insulin Resistance  Bone loss Muscle, and muscle building activity, or resistance training, has been shown to improve each and every one of these symptoms.  What's more, strength training surpasses cardio training in doing so. Cardio-induced stress is catabolic, meaning muscle breaks down at a faster rate.  There's more to love about muscle. It decreases inflammation. Inflammation that is linked to many diseases, particularly, Alzheimer's Disease (AD). Termed, type 3 diabetes, Alzheimer's is also a function of blood sugar. There's a direct correlation between amount of muscle mass and risk of AD and dementia. At age 65 a woman's risk of Alzheimer's is 1 in 5.  We are going to outlive men. We're going to need our strength to retain independence. Convinced? Here's how to know you're on the right path.  Measure How Much Muscle You Have Body composition can't be tracked by a scale alone. Invest in a Smart Scale, that is one that measures body fat percent at the least. If it gives you muscle mass in pounds or kgs, even better. You however can do the mass if you have weight and percent body fat.  Don't make the mistake of using BMI (Body Mass Index) as a measure of body composition. You don't know if your muscle is going up, down, or staying the same with BMI. When you know, you can modify exercise or lifestyle habits to support your muscle. It's better to know regularly than to find out annually or occasionally from the doctor or a gym. After 40 Muscle Building Tips Begin strength training twice weekly if you're not After a period of adaptation, reach temporary muscle fatigue each set  Begin with one set of weights you can lift 15-20 times  Progress after 1-2 weeks to weights you can only lift 12-15 times  Progress to two sets after 1-2 weeks Alternate this increase or either sets and or decrease repetitions  Maintain a regular 3 or more set strength training habit twice a week Prioritize sleep  Consume high quality protein throughout the day What Matters Most All of the exercise, nutrition, and lifestyle tips matter. But the greatest of these is strength training. That is, if you begin strength training without increasing protein intake or prioritizing sleep, you'll still benefit. Exercise is a catalyst for other health change however, so you may just find you sleep better because of the exercise, and that you're more conscious of your protein intake.  Work up to twice weekly total body sessions strength sessions with at least 3 sets of 8-10 muscle groups as heavy as you safely can. Watch your energy and overall Total Energy Expenditure (TEE) go up because you've increased strength without undue fatigue and soreness. For midlife women, this sweet spot for gaining lean muscle is the key to something that can be maintained for life, and that upgrades life. Long-term Wins with After 40 Muscle  When women strength train, their future changes for the better. Following exercise programs focused on resistance training rather than weight or fat loss, weight and body composition of postmenopausal women were maintained over a six-year period. By comparison, subjects with low levels of participation, or cardio-only programs, experience significant increases in weight, fat, and belly fat.   A midlife client once said to me, “I don't care what the question is, the answer is exercise.”  I couldn't agree more, but to be most accurate, for women over 50, its exercise with strength training as its foundation. You're Invited! The Online Event for Women Over 40: How to get and keep muscle, bone, and brain after 40:  https://www.flippingfifty.com/womensexercise Other Episodes You May Like:  5 Keys for Building Muscle After Menopause: https://www.flippingfifty.com/building-muscle-after-menopause/ The Genetics of Metabolism and Weight Loss for Women Over 40: https://www.flippingfifty.com/genetics-of-metabolism/  

News: Serum from hibernating black bears boosts muscle mass in human cells | New Atlas (01:16) The incredible ability of bears to hibernate for months at a time has inspired some interesting lines of research around how their secrets might benefit human health, and among them is a focus on muscle wasting. First let's talk about bear hibernation: The main difference between hibernation and torpor is during torpor, the animal is able to wake up quickly to avoid danger, or if the opportunity exists, exit the den to feed.  Hibernation is a voluntary state an animal enters to conserve energy, when food is scarce, and minimize exposure to the winter elements. During hibernation an animal lowers its body temperature, slows its breathing rate, heart rate, and metabolic rate-the rate its body uses energy. Bears technically do not hibernate, they enter a state similar to it called topor. Fun fact: Bears can sleep more than 100 days without eating, drinking, or passing waste! Bears can actually turn their pee into protein. Scientists in Japan have made a fascinating discovery in this space:Demonstrating how human muscle cells can be infused with serum from hibernating black bears to prevent atrophy and increase muscle mass. This new study focused on skeletal muscle, which is susceptible to wasting caused by immobility.Led by scientists at Hiroshima University and Hokkaido University The research team took cultured human skeletal muscle cells and infused them with serum drawn from the blood of hibernating black bears, which led to significant protein growth after 24 hours.Interestingly, serum collected during the bears' active summer season did not induce these same effects. Believe this is due to a factor in the hibernating bear serum that suppresses a "destruction mechanism" behind muscle degradation Study first-author Mitsunori Miyazaki, stated:“We have indicated that ‘some factor' present in hibernating bear serum may regulate protein metabolism in cultured human skeletal muscle cells and contribute to the maintenance of muscle mass … However, the identification of this 'factor' has not yet been achieved." Doing so could open up some exciting possibilities around protecting humans during deep space travel, or preventing muscle wastage in people who are immobile due to aging or disease.   Alzheimer's Breakthrough: Genetic Link to Gut Disorders Confirmed | Neuroscience News (08:18) A world-first Edith Cowan University (ECU) study has confirmed the link between the two, which could lead to earlier detection and new potential treatments.The findings add to the evidence the gut-brain axis may play a role in the development of neurodegenerative disorders. Alzheimer's Disease (AD), has no known curative treatments and is expected to affect more than 82 million people and is estimated to cost US$2 trillion by 2030. The study analyzed large sets of genetic data from AD and several gut-disorder studies – each of about 400,000 people.The first comprehensive assessment of the genetic relationship between AD and multiple gut disorders. They discovered people with AD and gut disorders have genes in common – which is important for many reasons. Research lead Dr Emmanuel Adewuyi explains:“The study provides a novel insight into the genetics behind the observed co-occurrence of AD and gut disorders … This improves our understanding of the causes of these conditions and identifies new targets to investigate to potentially detect the disease earlier and develop new treatments for both types of conditions.” When researchers conducted further analysis into the shared genetics, they found other important links between AD and gut disorders – such as the role cholesterol may play. Dr Adewuyi provides context:“Whilst further study is needed into the shared mechanisms between the conditions, there is evidence high cholesterol can transfer into the central nervous system, resulting in abnormal cholesterol metabolism in the brain… For example, elevated cholesterol in the brain has been linked to brain degeneration and subsequent cognitive impairment.” The research also indicated diet could play a part in treating and preventing AD and gut disorders.   There is a need for more studies and patients need to be assessed individually to judge whether they would benefit from cholesterol lower medication use.     This solar tower makes jet fuel from sunbeams, water, and gas | PopSci (14:43)  For the past several years, researchers from several different institutions in Switzerland and Germany have been using it to test a method to create propellantnormally a carbon-intensive process involving fossil fuels They use little more than sunlight and greenhouse gasses captured from the atmosphere. What happens inside their tower is a bit of chemistry known as the Fischer-Tropsch process.A collection of chemical reactions that converts a mixture of carbon monoxide and hydrogen or water gas into liquid hydrocarbons.  These reactions occur in the presence of metal catalysts Typically at temperatures of 150–300 °C (302–572 °F)  Pressures of one to several tens of atmospheres. So what does this structure tucked away in a Madrid suburb actually do?169 solar reflectors  concentrate blinding sunlight —on average, 2,500 times brighter than the sun—  to the top of a tower. It hits a porous ceramic box made from cerium, the rare-earth element number 58 That draws water and carbon dioxide from the air and splits their atoms into hydrogen gas and carbon monoxide. The newly created gasses sink to the bottom of the tower, where they enter a shipping container that carries out the Fischer-Tropsch reactions. The end result is fossil-fuel-free kerosene, produced by pulling carbon dioxide from the air.  The researchers say it can be pumped into fuel tanks, today, without issue. According to Aldo Steinfeld, an engineer at ETH Zürich in Switzerland, meeting the entire aviation's sector would require solar kerosene plants to cover an area of around 17,500 square miles, roughly the size of Estonia. That's large!!! Steinfeld looks at it differently: A relatively small parcel of a sparsely inhabited hot desert could supply all the world's planes.  The next steps are to make the process more efficient. Right now, a meager 4.1 percent of the solar energy striking the ceramic box actually goes into making gas.  The researchers think they could considerably boost that number.   Prime Air: Amazon officially rolls out drone delivery to customers | ZDNet (21:06) After years of development announcements, Amazon will be rolling out delivery by drone for Prime customers in areas of California and Texas.Lockeford, California, and College Station, Texas.  Amazon will join Walmart in offering limited drone delivery to a subset of customers, signaling a vote of confidence in the technology and a shifting regulatory environment from the two behemoth retailers. The service, called Prime Air, will deliver packages up to five pounds in less than an hour using drones. Fly up to 50 miles per hour (80km/hour), up to an altitude of 400ft, and can carry packages of up to 5lbs.  Created a proprietary sense-and-avoid system that enables Amazon drones to operate at greater distances while safely and reliably avoiding other aircraft, people, pets, and obstacles. Amazon is reaching out to customers in both locations to give them an option to receive free and fast drone delivery on what's billed as the largest selection of items ever to be available for drone delivery.Once onboarded, customers will see Prime Air-eligible items on Amazon Place an order as they normally would and receive an estimated arrival time The service will start later this year. Despite the limited rollout, the company's long-term vision is to create a drone delivery service that will scale and integrate into its vast fulfillment network.  Naturally, there's a lot more riding on these drones.A crash or injury involving an Amazon drone will receive heavy scrutiny. End it off with the end of Amazon's press release:“We're bringing more than drone delivery to Lockeford and College Station. Through these Prime Air drone deliveries, we will create new jobs, build partnerships with local organizations, and help to reduce the impact of climate change on future generations.”   A brain-computer startup beat Elon Musk's Neuralink to implanting its first device in a US patient | Yahoo (26:02) Synchron, a brain-computer interface startup, reportedly implanted its first device in a US patient earlier this month — overtaking Elon Musk's Neuralink for the third time.The startup implanted a 1.5-inch device into the brain of an ALS patient at Mount Sinai West medical center in New York on July 6 The purpose of the device is to allow the patient to communicate — even after they have lost the ability to move — by using their thoughts to send emails and texts. Should mention this company has already implanted the device in four patients in Australia who have been able to use the brain implant to send messages on WhatsApp and shop online. Last year, the Australia-based startup received permission from the US Food and Drug Administration (FDA) to begin human trials on six US patients who have been severely paralyzed.Neuralink has yet to receive FDA approval Synchon and Neuralink's implants have similar immediate applications. translate human thoughts into computer commands  could help patients with neurological diseases like Parkinson's or ALS. Neuralink and Synchron's products have several key differences: namely, size and installation. Synchron's device can be inserted into a human skull without cutting into it using a catheter, and the process requires two separate surgeries In contrast, Neuralink plans to make a much smaller and more powerful device that would require a portion of the individual's skull to be removed and would be performed using a robot ----more---- Social: Email Me: adam@thatscoolnew.com Twitter: @Thats_Cool_News   

The number of Americans living with Alzheimer's Disease (AD) continues to grow at an exponential rate. Currently, more than 6 million Americans have AD, and that number is expected to double by 2050. But recent research findings are beginning to show the important role diagnostics may play in the next era of AD. New diagnostic innovations could unleash a future of effective therapies, treatments, and improved outcomes for patients who suffer from this disease. In this episode, host Dr Pat Alagia, senior medical director for Women's and Reproductive Health at Quest Diagnostics, welcomes Dr Michael K. Racke to discuss: The current tools and methods available to physicians when diagnosing AD The important role of blood-based biomarkers in AD and the high impact this new testing solution can have on early diagnosis, as well as management of the disease Encouraging new treatments and diagnostic pathways for AD aiming to slow disease progression and improve quality of life Multilayered interventions to help prevent or delay risk of AD including a healthy diet, exercise, and cognitive stimulation   About our guests Dr Michael K. Racke is Medical Director for Neurology at Quest Diagnostics. He is a leader in the field of neurology and neuroimmunology with special expertise in multiple sclerosis.   After receiving his Doctor of Medicine from the University of Medicine and Dentistry of New Jersey, Dr Racke completed a medical internship and neurology residency at Emory University School of Medicine, followed by a neuroimmunology fellowship at the National Institute of Neurological Disorders and Stroke (NINDS) and the National Institutes of Health (NIH).   Dr Racke's research focuses on developing novel tests for neurologic disorders, including monitoring therapeutic responses in diseases such as multiple sclerosis. He has authored more than 200 peer-reviewed papers, book chapters, and reviews on the pathogenesis of neuroimmunology diseases. He has over 3 decades of leadership experience in academia and clinical practice and continues to serve on several national professional society committees.    Dr Racke is board certified by the American Board of Psychiatry and Neurology and is a member of the American Academy of Neurology and American Association of Immunologists.   ------------------------------ Quest Diagnostics empowers people to take action to improve health outcomes. Derived from the world's largest database of clinical lab results, our diagnostic insights reveal new avenues to identify and treat disease, inspire healthy behaviors, and improve healthcare management. Quest Diagnostics annually serves 1 in 3 adult Americans and half the physicians and hospitals in the United States, and our 47,000 employees understand that, in the right hands and with the right context, our diagnostic insights can inspire actions that transform lives. More information is available at www.QuestDiagnostics.com

Is your high blood sugar caused by electromagnetic hypersensitivity? Trent University (Ontario), June 1, 2022 Experts believe that the shocking epidemic of type 2 diabetes is being driven by lifestyle factors, primarily obesity and inactivity. But, evidence is accumulating that hypersensitivity to electromagnetic fields can cause high blood sugar, raising the possibility that a third form of the disease – “type 3 diabetes” – could be caused by this form of environmental pollution. Case studies show that high blood sugar is triggered by exposure to “dirty electricity” According to peer-reviewed research  published in Electromagnetic Biology and Medicine, “dirty electricity,” or transient electrical fields, can affect blood sugar levels in diabetic individuals who are electrically sensitive. Dr. Havas, an Associate Professor of Environmental and Resource Studies at Trent University, presented case studies showing that plasma glucose levels increased in response to electromagnetic pollution. Dr. Havas noted that people with unexplained rises in blood sugar could potentially be electrosensitive – and, in fact, suffering type 3 diabetes. (With 3 to 35 percent of the population experiencing electrosensitivity, as many as 5 to 60 million diabetics worldwide could be affected by this perplexing and under-diagnosed condition!) Electrosensitivity (ES), also known as electrical sensitivity, electromagnetic hypersensitivity and cellphone sickness, was originally termed “radio wave sickness.” It was officially identified in the 1970s by Russian doctors to describe an occupational syndrome developed by workers who were exposed to microwave or radiofrequency radiation. Symptoms occur when an individual is exposed to wireless technologies or electrical devices such as cell phone towers, “smart” meters, WiFi routers, power line magnetic fields, plasma TVs, laptops, cell phones, energy-efficient lighting, fluorescent lighting and dimmer switches. The symptoms can be mild or severe, and can include headaches, dizziness, heart palpitations, insomnia, memory problems, depression and fatigue. Numbness and tingling, high blood pressure, nosebleeds, tinnitus (ringing in the ears) and shortness of breath can also be indications of electrosensitivity. And, in spite of the item's name, you shouldn't work with a laptop on your lap. Avoiding smart meters, sleeping in an electricity-free bedroom, and eliminating dimmer switches are also wise moves, while installing Graham/Stetzer filters can help you cut down on “dirty electricity.” The takeaway: if you have been diagnosed with diabetes and are electrosensitive, cutting down on your EMF exposure is a commonsense choice you can make today.     A polyphenol-rich diet prevents inflammation in older people  University of Barcelona (Spain), June 8, 2022 Polyphenols in the foods that we eat can prevent inflammation in older people, since they alter the intestinal microbiota and induce the production of the indole 3-propionic acid (IPA), a metabolite derived from the degradation of tryptophan due to intestinal bacteria. This is stated in a study published in the journal Molecular Nutrition and Food Research, carried out by the Research Group at the University of Barcelona and the CIBER on Fragility and Healthy Ageing The study shows the interaction between polyphenols and gut microbiota can induce the proliferation of bacteria with the ability to synthetize beneficial metabolites, such as IPA, a postbiotic with antioxidant, anti-inflammatory and neuroprotective properties that contributes to improve the health of the intestinal wall. Therefore, this compound would contribute to the prevention of some diseases associated with ageing. “If we consider the beneficial effects of IPA on the gut microbiota and health in general, it is important to find reliable strategies to promote the production of this metabolite. As part of the study, the researchers carried out a multiomic analysis on faecal samples of fifty-one volunteers aged over sixty-five who kept following a diet rich in polyphenols (green tea, bitter chocolate, fruits including apples, pomegranate and blueberries) for eight weeks. The results show that the diet rich in polyphenols generated a significant increase in the blood IPA levels, together with a decrease in inflammation levels and changes in the bacteria of the microbiota, from the order of Bacteroidales.   Study shows people with a high omega-3 DHA level in their blood are at 49% lower risk of Alzheimer's Fatty Acid Research Institute, June 9, 2022 New research published today in Nutrients shows that people with a higher blood DHA level are 49% less likely to develop Alzheimer's disease vs. those with lower levels, according to the Fatty Acid Research Institute (FARI). The study, led by Aleix Sala-Vila, PhD, suggested that providing extra dietary omega-3 DHA, especially for those carrying the ApoE4 gene (which approximately doubles an individual's susceptibility to develop AD) might slow the development of the disease. Such a cost-effective, low-risk dietary intervention like this could potentially save billions in health care costs. In this prospective observational study conducted within the Framingham Offspring Cohort — including 1490 dementia-free participants aged ≥65 years old —  researchers examined the association of red blood cell (RBC) docosahexaenoic acid (DHA) with incident Alzheimer's Disease (AD), while also testing for an interaction with APOE-ε4 carriership. Tthe researchers noted that an increased intake of DHA might lower risk for developing AD, particularly in higher-risk individuals such as those carrying the APOE-ε4 allele, suggesting that they may benefit more from higher DHA levels than non-carriers.     Vegan diet rich in legumes beneficial for decreased weight in new study Physicians Committee for Responsible Medicine, June 8, 2022 A vegan diet improves diet quality, leading to decreased weight and improved insulin sensitivity, according to a new study by the Physicians Committee for Responsible Medicine published in the Journal of the Academy of Nutrition and Dietetics. Decreased weight was most associated with increased intake of legumes and decreased intake of meat, fish, and poultry. “Our research shows that the best way to improve the quality of your health is to improve the quality of the foods you eat,” says Hana Kahleova, MD, PhD, director of clinical research at the Physicians Committee and a study co-author. “That means avoiding animal products and eating a vegan diet rich in fruits, vegetables, grains, and beans.” The participants in the 16-week study included 244 overweight adults who were randomly assigned to either make no diet changes or to follow a low-fat vegan diet, without calorie restrictions, consisting of vegetables, grains, legumes, and fruits. Researchers tracked diet quality, body weight, fat mass, and insulin sensitivity. The final data analysis included 219 participants who completed the whole study and submitted their final diet records. Participants on the vegan diet lost an average of 13 pounds and 9.1 pounds of fat mass. Body weight and fat mass did not decrease in the group that made no diet changes. In the vegan group, increases in fruit, legume, meat alternative, and whole grain intake and decreases in animal products, added oils, and animal fats were associated with weight loss: Fruit: Increased intake of whole fruit was associated with a decrease in body weight. Legumes and Meat Alternatives: Increased legume consumption was associated with decreased weight, fat mass, and visceral adipose tissue. Consuming more meat alternatives, including tofu, tempeh, and veggie burgers, was associated with a decrease in body weight. Grains: Increased consumption of whole grains was associated with decreased body weight and fat mass. Eggs and Dairy Products: Decreased egg intake was correlated with decreased weight. Decreased high-fat dairy intake was associated with decreased weight and fat mass. Meat, Fish, and Poultry: Reductions in the combined intake of total meat, fish, and poultry were associated with weight loss and a decrease in fat mass. Added Fats: Decreases in intake of added animal fats were associated with decreases in weight and fat mass. Decreased intake of added oils also correlated with decreases in weight and fat mass. The vegan group also experienced improvements in insulin sensitivity.   Western diets rich in fructose and fat cause diabetes via glycerate-mediated loss of pancreatic islet cells Terasaki Institute for Biomedical Innovation, June 9, 2022   Those who are habitually inclined to consume burgers, fries and soda may think twice about their dietary choices following scientists' latest findings about high-fat, high-fructose diets. As reported in their recent publication in Cell Metabolism, the Terasaki Institute for Biomedical Innovation (TIBI), discovered that a high-fat diet can increase fructose metabolism in the small intestine, leading to release of a fructose-specific metabolite called glycerate into circulation. Circulating glycerate can subsequently cause damage of the insulin-producing pancreatic beta cells, increasing the risk of glucose tolerance disorders, such as Type 2 diabetes mellitus (T2DM). Although T2DM is typically found in older people, it has been occurring more and more in younger people. In the past two decades alone, T2DM has doubled in prevalence. Equally concerning are the health risks associated with T2DM, including heart disease and stroke.  In T2DM, there are insufficient levels of insulin, a hormone that regulates movement of glucose into peripheral cells. To compensate for this, the pancreas overworks to secrete additional insulin, with eventual loss of this ability. The result is an unhealthy accumulation of glucose in the blood. Collectively, the scientists' findings suggest that a prolonged exposure to high levels of glycerate due to excessive consumption of western diets rich in dietary fructose and fat poses the risk of damage to the pancreatic islet cells and development of diabetes.   New study associates intake of dairy milk with greater risk of prostate cancer Loma Linda University, June 9, 2022   Men with higher intakes of dairy foods, especially milk, face a significantly higher risk of prostate cancer compared to men with lower intakes, according to a new study conducted by researchers at Loma Linda University Health. The study found no such associations between increased prostate cancer risk and intake of non-dairy calcium, suggesting substances other than calcium play a role in the risk dairy foods poses for prostate cancer. The study's results reveal that men who consumed about 430 grams of dairy per day (1 ¾ cups of milk) faced a 25% increased risk of prostate cancer compared to men who consumed only 20.2 grams of dairy per day (1/2 cup of milk per week). Also, men who consumed about 430 grams of dairy per day faced an even greater increase in risk when compared to men with zero dairy intake in their diets. Fraser noted that the results had minimal variation when comparing intake of full fat versus reduced or nonfat milks; there were no important associations reported with cheese and yogurt.  

CME credits: 0.50 Valid until: 19-05-2023 Claim your CME credit at https://reachmd.com/programs/cme/qad-addressing-challenges-in-alzheimers-disease-from-early-identification-to-new-treatment-considerations/13485/ Alzheimer's Disease (AD) is a progressive disease that presents challenges when it comes to the early diagnosis and treatment of patients. That's why this two-part series will help answer your specific questions while providing expert insights into these challenges. In this first activity, a panel of esteemed faculty will examine the case of a patient who was diagnosed early with mild cognitive impairment (MCI) due to AD, prior to dementia. Using this patient case, faculty will delve into both the importance of early identification of AD and how to detect it early. The panel will then discuss the pathobiology of AD and potential treatments in development to target this pathology. Finally, the panel will explore current treatment options, including the appropriate use of anti-amyloid monoclonal antibody (mAb) treatment. Throughout this activity, we will gather questions from clinicians like you who care for patients living with dementia, and then in part two of this series, we will answer some of the questions generated from this first activity.

CME credits: 0.50 Valid until: 19-05-2023 Claim your CME credit at https://reachmd.com/programs/cme/qad-addressing-challenges-in-alzheimers-disease-from-early-identification-to-new-treatment-considerations/13485/ Alzheimer's Disease (AD) is a progressive disease that presents challenges when it comes to the early diagnosis and treatment of patients. That's why this two-part series will help answer your specific questions while providing expert insights into these challenges. In this first activity, a panel of esteemed faculty will examine the case of a patient who was diagnosed early with mild cognitive impairment (MCI) due to AD, prior to dementia. Using this patient case, faculty will delve into both the importance of early identification of AD and how to detect it early. The panel will then discuss the pathobiology of AD and potential treatments in development to target this pathology. Finally, the panel will explore current treatment options, including the appropriate use of anti-amyloid monoclonal antibody (mAb) treatment. If you would like to view the second part of this series, please click here.

See all the Healthcasts at https://www.biobalancehealth.com/healthcast-blog/ I have always told women who are menopausal that giving Estrogen to them after menopause lower's their risk of Alzheimer's, decreases their insulin resistance and helps decrease belly fat.  There are many studies that prove that testosterone decreases the risk of Alzheimer's Disease (AD) and delays the timing of AD by 10 years.  This is what I have always told women to reassure them about taking estrogen and testosterone after their ovaries stop making both hormones.  It is a simple concept that the practice of medicine has made very complex, however this new research article in Nature 3-2022 by Dr Kamoroff, helps support the practice of replacing the hormones that women lose with menopause, estrogen and testosterone, to prevent the diseases of aging including Osteoporosis and Dementia. Let me explain the response of the female body to our ovaries shrinking and essentially dying, which is what women's ovaries do when we become menopausal. The ovaries are the primary source of estradiol (young women's estrogen) and the only secretor of testosterone in women.  Other androgens are produced by the adrenal gland, but they do not provide a woman with the benefits of pure testosterone. At menopause blood levels of estradiol (E2) decrease to nearly zero. Free T (the active form of T), and estradiol also decreases to less than 60 pg/dl from a pre-menopausal range of 60-250 pg/dl.   In response to this radical change in a woman's chemistry, and very low levels of Estradiol and Testosterone, the pituitary raises the FSH and LH production, the hormones that, previous to menopause stimulated the ovaries to make more E2 and T. After menopause the increasing of FSH and LH continues to increase and cause hot flashes and night sweats.  These two hormones are only suppressed by a woman replacing Estrogen and or Testosterone (T). When women get E2 and T, it causes the FSH and LH to “relax” and stop sending out high levels, so hot flashes and night sweats stop.  If E and T are not replaced, LH and FSH continue to be elevated and these symptoms can continue for life! This most recent study by Dr. Kamaroff goes one step farther toward what I already know about ERT (estrogen replacement therapy), and just described. The only way to stop the cause of elevated FSH and LH, and hot flashes and night sweats, is the replacement of estrogen and testosterone. Giving enough estrogen to achieve pre-menopausal blood levels of these two hormones is to give higher doses than the FDA approves of.  It is our goal to prevent AD, dementia and Osteoporosis my dosing adequate Estradiol and Testosterone in the form of subcuticular pellets.  Low dose estradiol is not the way to be healthy after menopause.  Women need adequate hormones to shut down the FSH and LH surges and that is the way to prevent several of the diseases of aging. Simply, this new study links the elevation of FSH and LH to the onset of dementia, Alzheimer's Disease and Osteoporosis (thinning of bones) after menopause. But how does FSH and LH cause dementia and Alzheimer's disease? This study blames the elevation of FSH and LH for causing inflammation and the accumulation of B amyloid on neurons in the brain is a response to inflammation. This accumulation of plaque causes Alzheimer's Disease (AD). It seems that the recommendation of the American College of OBGYN gives to doctors to limit the dose and the time ERT and HT are given is counterproductive to the health of women's brains and bones.  The result is that most women are given too little estrogen, and therefore are still at moderate risk for AD and Osteoporosis.   When we give compounded E2 and T with pellets, the FSH and LH are suppressed to pre-menopausal levels, and therefore it is the best way to prevent hot flashes but also prevent osteoporosis and AD that can develop without a sufficient amount of estrogen.  It is in this way that women without ERT or who have low dose estrogen replacement oral, or patch have a higher risk of the diseases of aging, AD and Osteoporosis than those women who are given an adequate dose that provides pre-menopausal blood levels. A second study reported at the American Heart Association's Epidemiology, Prevention, Lifestyle & Cardiometabolic Health Conference 2022, also reported that the longer a woman is without estrogen, the higher her risk of developing heart disease and dementia. This is consistent with the first study I cited, that links high LH and FSH to these diseases of aging. This study looked at women who go through menopause early, before 40, who therefore have more years of high LH and FSH, and a longer period of time associated with inadequate estradiol and testosterone. The earlier women experience menopause the higher the incidence of Dementia by 1.3 times the rate of women who went through menopause at the normal time, after age 40. The healthier aging without disease occurred in women who had more exposure to Estradiol and Testosterone, and less exposure to elevated FSH and LH. The bottom line for both research studies is that estradiol is one of the keys to healthy aging, pivotal to preventing the devastating diseases of aging like Osteoporosis, Heart Disease, and Dementia. Estradiol is a hormone that should NOT be dosed to achieve a minimal blood level, and when it is replaced after menopause with reasonable doses meant to achieve a normal physiologic blood level , this one hormone brings a woman's body back to homeostasis and can lead to healthy aging without the diseases of aging. March 22, 2022 Follicle-Stimulating Hormone's Role in Alzheimer Disease, in Mice Anthony L. Komaroff, MD, reviewing Xiong J et al. Nature 2022 Mar Blocking FSH in ovariectomized mice protected against cognitive decline. The incidence of Alzheimer disease (AD) is particularly high in older women, as are levels of follicle-stimulating hormone (FSH). This observation led investigators to wonder whether blocking the action of FSH might be beneficial. In mouse models of AD, ovariectomy (with its associated sharp rise in FSH level) promptly increases the degree of deposition of both β-amyloid and tau, which are cardinal pathologic features of AD. Following ovariectomy in mice, the researchers administered a monoclonal antibody that blocked the action of FSH. The antibody reduced deposition of both β-amyloid and tau in the brain and protected against cognitive decline. The mechanism for this effect is that blocking FSH also blocks an enzyme that causes accumulation of both β-amyloid and tau. Further incriminating FSH in AD pathology, deposition of β-amyloid and tau also was reduced by using genetic engineering to knock out receptors for FSH, and deposition was increased by raising levels of FSH. FSH also is produced at low levels in males, and the FSH-blocking antibody also reduced hippocampal and cortical deposition of β-amyloid and tau in males. Experiments showed that two other features of menopause — low estrogen levels and high luteinizing hormone levels — did not explain the AD-like features seen in ovariectomized mice. COMMENT Many, but not all, findings in mouse models of AD have been replicated in humans. Blocking FSH also reduced bone loss and visceral fat in mice. Given all these theoretical benefits, one might surmise that trials of FSH blockade in humans will be undertaken. Study: Early menopause may signal women's dementia risk A preliminary study to be presented at the American Heart Association's Epidemiology, Prevention, Lifestyle & Cardiometabolic Health Conference 2022 found that women who experience menopause before they reach 40 years of age may have a 35% increased risk for dementia later in life. The researchers also found that women who entered menopause before they turned 45 years old were 1.3 times more likely to receive an early dementia diagnosis by the time they reach 65 years of age.

Kellyann Niotis, M.D., discusses Alzheimer's Disease (AD). She shares the genetic risk factors for developing AD and the age at which many people may begin to exhibit symptoms. She discusses some of the recent advancements in treating AD and the ongoing research towards finding a cure. Finally, she provides some behavioral strategies for patients and their loved ones for optimizing memory and cognitive functions.To schedule an appointment with Kellyann Niotis, M.D.

Hideki Garren, MD, PhD, Chief Medical Officer at Prothena discusses data from two presentations at the Alzheimer's Association International Conference (AAIC); PRX012, Prothena's next generation anti-amyloid beta (Aβ) antibody and the dual Aβ-tau vaccine being developed for the prevention and treatment of Alzheimer's Disease (AD). He talks about the company's approach to addressing the AD global healthcare crisis. #Alzheimer #AAIC H​ideki Garren, M.D., Ph.D.​, Chief Medical Officer​. Dr. Garren has served as our Chief Medical Officer since April 2021. Before joining Prothena, between 2013 and 2021 Dr. Garren was with F. Hoffmann-La Roche Ltd. (Roche) & Genentech Inc. and most recently served as Vice President, Global Head of Neuroimmunology with responsibility for leading Roche's Neuroimmunology franchise team. Prior to Roche, between 2011 and 2013, Dr. Garren held the role of Executive Director, Translational Medicine Expert in Neuroscience with Novartis Pharma. Dr. Garren also served as Co-Founder, Executive Vice President, Chief Scientific Officer, and Chief Operating Officer of Bayhill Therapeutics, Inc., a company he started in 2002 based on a technology platform he co-invented while at Stanford University. He currently serves on the board of directors of Coya Therapeutics, a privately-held clinical-stage biotechnology company. Dr. Garren earned his Bachelor of Science from the California Institute of Technology and his MD and PhD from the University of California, Los Angeles (UCLA). He completed his internship in internal medicine at UCLA, and his residency in neurology and fellowship in neuroimmunology at Stanford University.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.11.20.390435v1?rss=1 Authors: Karimi, H., Marefat, H., Khanbagi, M., Kalafatis, C., Modarres, M. H., Vahabi, Z., Khaligh-Razavi, S.-M. Abstract: Electroencephalography (EEG) has been commonly used to measure brain alterations in Alzheimer's Disease (AD). However, reported changes are limited to those obtained from using univariate measures, including activation level and frequency bands. To look beyond the activation level, we used multivariate pattern analysis (MVPA) to elicit the pattern of information processing from EEG responses to an animacy categorization task. Comparing healthy controls (HC) with patients with mild cognitive impairment (MCI), we found that the neural speed of animacy information processing is decreased in MCI patients. Moreover, we found critical time-points during which the representational pattern of animacy for MCI patients was significantly discriminable from that of HC, while the activation level remained unchanged. Together, these results suggest that the speed and pattern of animacy information processing provide clinically useful information as a potential biomarker for detecting early changes in MCI and AD patients. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.10.06.327833v1?rss=1 Authors: Haytural, H., Jorda-Siquier, T., Winblad, B., Mulle, C., Tjernberg, L. O., Granholm, A.-C., Frykman, S., Barthet, G. Abstract: Synaptic degeneration has been reported as one of the best pathological correlate of cognitive deficit in Alzheimer's Disease (AD). However, the location of these synaptic alterations within hippocampal sub-regions, the vulnerability of the presynaptic versus postsynaptic compartments, and the biological mechanisms for these impairments remain unknown. Here, we performed immunofluorescence labeling of different synaptic proteins in fixed and paraffin embedded human hippocampal sections and report reduced levels of several presynaptic proteins of the neurotransmitter release machinery (complexin-1, syntaxin-1A, synaptotagmin-1 and synaptogyrin-1) in AD cases. The deficit was restricted to the outer molecular layer (OML) of the dentate gyrus whereas other hippocampal sub-fields were preserved. Interestingly, standard markers of postsynaptic densities (SHANK2) and dendrites (MAP2) were unaltered, as well as the relative number of granule cells in the dentate gyrus, indicating that the deficit is preferentially presynaptic. Notably, staining for the axonal components, myelin basic protein, SMI-312 and Tau, was unaffected, suggesting that the local presynaptic impairment does not result from axonal loss or alterations of structural proteins of axons. There was no correlation between the reduction in presynaptic proteins in OML and the extent of the amyloid load or of the dystrophic neurites expressing phosphorylated forms of Tau. Altogether, this study highlights the distinctive vulnerability of the OML of dentate gyrus and supports the notion of presynaptic failure in AD. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.06.18.158980v1?rss=1 Authors: Roe, J. M., Vidal-Pineiro, D., Sorensen, O., Brandmaier, A. M., Duzel, S., Gonzalez, H. A., Kievit, R. A., Knights, E., Kuhn, S. A., Lindenberger, U., Mowinckel, A. M., Nyberg, L., Park, D. C., Pudas, S., Rundle, M. M., Walhovd, K. B., Fjell, A. M., Westerhausen, R. Abstract: Normal aging and Alzheimer's Disease (AD) are accompanied by large-scale alterations in brain organization that undermine brain function. Although hemispheric asymmetry is a global organizing feature of cortex thought to promote brain efficiency, current descriptions of cortical thinning in aging and AD have largely overlooked cortical asymmetry. Consequently, the foundational question of whether and where the cerebral hemispheres change at different rates in aging and AD remains open. First, applying vertex-wise data-driven clustering in a longitudinal discovery sample (aged 20-89; 2577 observations; 1851 longitudinal) we identified cortical regions exhibiting similar age-trajectories of asymmetry across the adult lifespan. Next, we sought replication in 4 independent longitudinal aging cohorts. We show that higher-order regions of cortex that exhibit pronounced asymmetry at age ~20 also show asymmetry change in aging. Results revealed that both leftward and rightward asymmetry is progressively lost on a similar time-scale across adult life. Hence, faster thinning of the (previously) thicker homotopic hemisphere is a feature of aging. This simple organizational principle showed high consistency across multiple aging cohorts in the Lifebrain consortium, and both the topological patterns and temporal dynamics of asymmetry-loss were markedly similar across replicating samples. Finally, we show that regions exhibiting gradual asymmetry-loss over healthy adult life exhibit faster asymmetry-change in AD. Overall, our results suggest a system-wide breakdown in the adaptive asymmetric organization of cortex across adult life which is further accelerated in AD, and may implicate thickness asymmetry as a viable marker for declining hemispheric specialization in aging and AD. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.06.17.154104v1?rss=1 Authors: Jonin, P.-Y., Duche, Q., Bannier, E., Corouge, I., Ferre, J.-C., Belliard, S., Barillot, C., Barbeau, E. J. Abstract: Impaired memory is a hallmark of prodromal Alzheimer's Disease (AD). Prior knowledge associated with the memoranda has proved to have a powerful effect on memory in healthy subjects. Yet, barely nothing is known about its effect in early AD. We used functional MRI to ask whether prior knowledge enhanced memory encoding in early AD and whether the nature of prior knowledge mattered. Early AD patients and healthy controls underwent a task-based fMRI experiment, being scanned while learning face-scene associations. Famous faces carried Pre-Experimental Knowledge (PEK) while unknown faces repeatedly familiarized prior to learning carried Experimental Knowledge (EK). As expected, PEK increased subsequent memory in healthy elderly. However, patients did not benefit from PEK. Partly non-overlapping brain networks supported PEK vs. EK encoding in healthy controls. Patients displayed impaired activation in a right subhippocampal region where activity predicted successful associative memory formation of PEK stimuli. These findings call for a thorough consideration of how prior knowledge impacts learning and suggest a possible underestimation of the extent of associative memory impairment in early AD. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.06.17.157552v1?rss=1 Authors: Abreha, M. H., Ojelade, S., Dammer, E. B., McEachin, Z. T., Duong, D. M., Gearing, M., Bassell, G. J., Lah, J. J., Levey, A. I., Shulman, J. M., Seyfried, N. T. Abstract: One of the defining pathological features of Alzheimer's Disease (AD) is the deposition of neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau in the brain. Aberrant activation of kinases in AD has been suggested to enhance phosphorylation and toxicity of tau, making the responsible tau-directed kinases attractive therapeutic targets. The full complement of tau interacting kinases in AD brain and their activity in disease remains incompletely defined. Here, immunoaffinity enrichment coupled with mass spectrometry (MS) identified TANK-binding kinase 1 (TBK1) as a tau-interacting partner in human AD cortical brain tissues. We validated this interaction in both human AD and familial frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) caused by mutations in MAPT (R406W) postmortem brain tissues as well as human cell lines. Further, we document increased TBK1 activity in both AD and FTDP-17 and map the predominant TBK1 phosphorylation sites on tau based on in vitro kinase assays coupled to MS. Lastly, in a Drosophila tauopathy model, activating expression of a conserved TBK1 ortholog triggers tau hyperphosphorylation and enhanced neurodegeneration, whereas knockdown had the reciprocal effect, suppressing tau toxicity. Collectively, our findings suggest that increased TBK1 activity may promote tau hyperphosphorylation and neuronal loss in AD and related tauopathies. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.05.15.098749v1?rss=1 Authors: Rodriguez, S., Hug, C., Todorov, P., Moret, N., Boswell, S. A., Evans, K., Zhou, G., Johnson, N. T., Hyman, B., Sorger, P., Albers, M. W., Sokolov, A. Abstract: Clinical trials of novel therapeutics for Alzheimer's Disease (AD) have consumed a large amount of time and resources with largely negative results. Repurposing drugs already approved by the Food and Drug Administration (FDA) for another indication is a more rapid and less expensive option. Repurposing can yield a useful therapeutic and also accelerate proof of concept studies that ultimately lead to a new molecular entity. We present a novel machine learning framework, DRIAD (Drug Repurposing In AD), that quantifies potential associations between the pathology of AD severity (the Braak stage) and molecular mechanisms as encoded in lists of gene names. DRIAD was validated on gene lists known to be associated with AD from other studies and subsequently applied to evaluate lists of genes arising from perturbations in differentiated human neural cell cultures by 80 FDA-approved and clinically tested drugs, producing a ranked list of possible repurposing candidates. Top-scoring drugs were inspected for common trends among their nominal molecular targets and their "off-targets", revealing a high prevalence of kinases from the Janus (JAK), Unc-51-like (ULK) and NIMA-related (NEK) families. These kinase families are known to modulate pathways related to innate immune signaling, autophagy, and microtubule formation and function, suggesting possible disease-modifying mechanisms of action. We propose that the DRIAD method can be used to nominate drugs that, after additional validation and identification of relevant pharmacodynamic biomarker(s), could be evaluated in a clinical trial. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.04.24.060558v1?rss=1 Authors: Paranjpe, M. D., Belonwu, S., Wang, J. K., Oskotsky, T., Gupta, A., Taubes, A., Zalocusky, K., Paranjpe, I., Glicksberg, B. S., Huang, Y., Sirota, M. Abstract: In spite of evidence of females having a greater lifetime risk of developing Alzheimer's Disease (AD) and greater apolipoprotein E4-related (apoE4) AD risk compared to males, molecular signatures underlying these findings remain elusive. We took a meta-analysis approach to study gene expression in the brains of 1,084 AD patients and age-matched controls and whole blood from 645 AD patients and age-matched controls. Gene-expression, network-based analysis and cell type deconvolution approaches revealed a consistent immune signature in the brain and blood of female AD patients that was absent in males. Machine learning-based classification of AD using gene expression from whole blood in addition to clinical features revealed an improvement in classification accuracy upon stratifying by sex, achieving an AUROC of 0.91 for females and 0.80 for males. These results help identify sex and apoE4 genotype-specific transcriptomic signatures of AD and underscore the importance of considering sex in the development of biomarkers and therapeutic strategies for AD. Copy rights belong to original authors. Visit the link for more info

Has Alzheimer's Disease has touched your family? There are 50,000 Utahns affected by Alzheimer's Disease (AD) and Utah has the nation's highest growth rate of AD (127%). There are more than 5 million cases of AD in the US today and by 2050, that number is expected to nearly triple to 13.8 million and care costs will reach over $1.2 trillion. There is no known cure and the impact on afflicted individuals and their families is devastating. The AD process may begin decades before diagnosis. But Maria Norton, USU Associate Professor of Family Consumer and Human Development, says that while there are some factors we are born with (e.g. genes) that can't be modified, there are a host of factors that have been shown to affect our risk for Alzheimer's that ARE modifiable, and if we can encourage individuals, families and communities to adopt healthy lifestyle habits, we may be able to make a "course correction" to avoid or at least delay AD as individuals, and as a society.