Tips for Understanding Neurodegenerative Diseases

Your brain starts changing up to 20 years before the first tremor appears. As a neuropsychiatrist specialized in neurodegeneration, I've seen how our understanding has evolved. Parkinson's was long considered just a "movement disorder," separate from dementia. We now know it's part of the same neurodegenerative family as other dementias. In fact, Parkinson's and Lewy body dementia are essentially the same disease process—just affecting different brain regions at different times. Working with hundreds of patients, I've heard the same story countless times: "Looking back, the signs were there—I just didn't recognize them." Research now confirms these subtle warnings can appear 5-20 years before clinical diagnosis. Here are 5 early signs to watch for: 1/ Loss of smell ability (anosmia) ↳ Often the earliest signal, appearing 20+ years before diagnosis ↳ Studies show that more than 95% of patients with Parkinson's disease present with significant olfactory loss preceding movement symptoms by years ↳ Many don't notice the change or attribute it to aging ↳ Affects ability to detect specific scents like bananas, dill pickles, or licorice 2/ REM sleep behavior disorder (RBD) ↳ Physically acting out dreams, often violently ↳ Research shows over 70% of patients with RBD will develop parkinsonism or dementia within 12 years of their diagnosis ↳ Bed partners report being kicked, punched, or yelled at during sleep ↳ Often mistaken for ordinary nightmares or restlessness 3/ Persistent constipation ↳ This symptom often appears many years ahead of movement symptoms ↳ Not responsive to typical remedies or lifestyle changes ↳ Often dismissed as diet-related or normal aging ↳ Indicates early dysfunction in the gut-brain connection 4/ Micrographia (small handwriting) ↳ Cramped, small handwriting — called micrographia — is one of the early symptoms ↳ May start gradually with writing becoming progressively smaller ↳ Often noticed by others before the person writing ↳ Can appear years before diagnosis 5/ Depression or anxiety without clear cause ↳ Depression can appear years or even decades before movement symptoms ↳ Often late-onset without previous history ↳ More persistent than situational depression ↳ Higher rates of anxiety in early Parkinson's than general population These symptoms aren't definitive proof of Parkinson's— but seeing multiple signs should prompt a conversation with a healthcare provider. The silver lining? Earlier detection means earlier intervention, which may help slow progression and preserve quality of life. —----------------------------- ⁉️ Did you know Parkinson's and Lewy Body Dementia were the same disease? Let me know in the comments below. ♻️ Repost to help others recognize these early warning signs. 👉 Follow me (Reza Hosseini Ghomi, MD, MSE) for more like this.

🧠 Is Alzheimer’s Really Type 3 Diabetes? The Surprising Link Between Metabolic Health and Cognitive Decline If you’ve ever heard Alzheimer’s disease referred to as “Type 3 Diabetes,” it’s not just a catchy phrase, it’s a warning backed by a growing body of science. And the implications are massive. What Does This Mean? We know that insulin isn’t just about blood sugar — it’s also critical for brain function. In fact, your brain uses more energy than any other organ in your body, and glucose is its primary fuel source. But here’s the catch: 🔬 When the body becomes insulin resistant… the brain does too. And when brain cells can’t properly respond to insulin or access glucose for energy, they begin to starve. This cellular dysfunction contributes to memory loss, impaired cognition, and eventually the hallmarks of Alzheimer’s, including amyloid plaques and tau tangles. 📚 Clinical Evidence Is Mounting A number of peer-reviewed studies now point to insulin resistance as a key driver in neurodegeneration: The Journal of Alzheimer's Disease (2016) stated: "Insulin resistance and deficiency are common in Alzheimer’s and contribute to cognitive decline." Mayo Clinic Proceedings (2012) found that people with higher insulin resistance in midlife had significantly higher risk of developing Alzheimer’s later. Neurobiology of Aging (2005) introduced the term “Type 3 Diabetes” to describe Alzheimer’s as a form of insulin resistance localized in the brain. 🧬 Alzheimer’s may not be a disease of aging. It may be a disease of metabolic dysfunction. And here’s the truly hopeful part: Insulin resistance can be reversed, naturally. ✅ 5 Research-Backed Strategies to Protect Your Brain You don’t need a diagnosis to take action. Here are five powerful, proven ways to support insulin sensitivity and protect cognitive function: 🍽️ Practice Intermittent Fasting Reduces insulin levels, promotes autophagy, and allows the brain to clear damaged cells. 🚶 Move After Meals Even a 10-minute walk can significantly improve glucose uptake and lower post-meal insulin spikes. 🥩 Prioritize Protein & Healthy Fats Swap refined carbs for whole foods that nourish the brain and stabilize blood sugar. 🌞 Get Sunshine & Prioritize Sleep Vitamin D and deep sleep are both critical for hormonal balance and brain detoxification. 🧘 Manage Chronic Stress Stress raises cortisol and insulin. Daily breathwork, nature, or journaling can help. 🗣 Let’s Shift the Conversation Alzheimer’s is now the fifth leading cause of death for adults over 65. But if we can reframe it as a preventable metabolic condition, rather than an inevitable part of aging, we can empower millions to take control of their health before symptoms ever appear. Have you heard Alzheimer’s referred to as Type 3 Diabetes? What are your thoughts on this connection? 👇 I’d love to hear your perspective.

What if the best time to prevent cognitive decline (and even Alzheimer’s) is decades before symptoms appear? A groundbreaking new study in PNAS found that brain aging is rapidly accelerating by the fifth decade of life, driven by neuronal insulin resistance. Around this time, neurons start to experience impaired glucose uptake, leading to cellular and network dysfunction and a cascade of subsequent inflammation and vascular damage. The process kicks off around age 44, peaks at about age 67, and is plateauing by age 90. But there’s good news: At early stages, delivery of ketones can shift the dysfunction back towards a normal state since ketones are taken up by neurons by a different, insulin-independent route that is still intact (could creatine do something similar?). At later stages, too much damage has accumulated for this intervention to have much effect. This is a massive study (fMRI from over 19K participants!) with a lot to digest. But there are a few key takeaways: 🧠 Metabolic dysfunction kicks off network dysfunction in the brain in your mid-40s. 🩺 This likely initiates the complex damage processes that we recognize as neurodegeneration and neuroinflammation, which manifest as cognitive decline or dementia later in life. ⏪ Correcting metabolic dysfunction could prevent this cascade from progressing, but this is only possible in the earlier stages of the process. 💊 Ketones are a helpful bandaid. Other interventions that restore brain insulin sensitivity (SGLT2 inhibitors, exercise, etc.) could be much more helpful and sustainable. Addressing brain health at midlife isn't just wise—it might be essential. 📰 Link to full study in the comments. #BrainHealth #Longevity #Healthspan #Metabolism #fMRI #Neurodegeneration #Dementia #Cognitivedecline #Aging

What happens when there is rust in the brain's wires and cells? We continue to struggle with understanding iron and neuroferroptosis and whether there will be an 'iron age' of the brain and disease? The just published paper in Nature Reviews Neuroscience by Lei, Walker and Layton makes the case that our aging brains accumulate iron like rust on a wire. The buildup, if left unchecked, can trigger cell death referred to as neuroferroptosis. This isn’t just theory, it's a process that could underlie Parkinson's, Alzheimer's, ALS, stroke, and brain cancer. Key Points: - The way the brain is built it is at high risk for the effects of iron. It's lipid-rich, iron-loaded, and oxygen-hungry. - These represent a 'perfect storm' of conditions for ferroptosis, an iron-dependent, lipid-peroxidizing cell death pathway. - Neurons possess a massive membrane surface and limited self-renewal capacity. Their defenses rely on selenium, GPX4, glutathione, and antioxidants like vitamin E. They are thus very susceptible. - The connective tissue of the brain, the microglia, can spread the process. When microglia undergo ferroptosis, they activate astrocytes and propagate damage to neurons. - Once started, the process triggers and propagates neuroinflammation and degeneration. - Elevated iron, reduced antioxidants, and genetic risk factors all link neuroferroptosis to Alzheimer's, Parkinson's, ALS, stroke, MS, and neurodegeneration w/ iron accumulation disorders. - Chelating or removing the iron may actually backfire. Iron is essential for brain metabolism and dopamine production. Trials using iron chelators worsened outcomes in Alzheimer's and Parkinson's. My take: I have 3 big takeaways: 1- Iron is a double-edged sword. We need it for brain health, however too much can rust the brain’s wiring, leading to a worrisome cascade of damage. 2- Cell death isn’t just a final act, it actually may start earlier than you think. Neuroferroptosis likely begins long before symptoms of Parkinson’s or Alzheimer’s appear. 3- Antioxidants and selenium may matter, however remember, they are not magic bullets. Nutrients like vitamin E and selenium help protect the brain, but we’ll need smarter, targeted therapies to truly make a dent in neuroferroptosis. This gives us one more reason to take one multivitamin a day until we sort out the specifics. https://lnkd.in/ebA4YmpY Nature Magazine Norman Fixel Institute for Neurological Diseases Parkinson's Foundation Alzheimer's Association® The ALS Association

What is the difference between Parkinson’s and Alzheimer’s? To answer this question and more, I spoke with Ayesha Sherzai, MD, MAS, neurologist and co-director of the Alzheimer’s Prevention Program at Loma Linda University Health. Watch the clip and/or read a detailed answer below. And catch the full discussion here: https://shorturl.at/NkZjC. First, what's similar? They both, of course, impact the brain -- but in different areas and in different ways. Brain cells are damaged or die, which is why they are called "neurodegenerative" diseases. The symptoms gradually worsen over time. There isn't yet a way to stop progression or to cure these diseases, although there are many medications and treatments to lessen symptoms. What about the symptoms? Alzheimer's causes memory loss and thinking changes -- forgetting recent events, getting lost in familiar places or while driving, not being able to learn or process new activities. Parkinson's causes movement changes -- tremor (shaking), slowness, stiffness and others. But, Parkinson's can also impact memory and thinking. This doesn't happen for everyone and can range from subtle and barely noticeable to significant and impacting daily life. Similarly, Alzheimer's can, especially later on, impact movement -- causing a person to move more slowly, for example. What causes them? Aging is the biggest risk for both. But that does not mean these diseases are a normal or expected part of getting older. Genetics and environmental factors also play a role. Each involves normal proteins that fold abnormally and clump in the brain. For Parkinson's that's alpha-synuclein and for Alzheimer's, the proteins are beta-amyloid and tau. But sometimes people with Parkinson's have "Alzheimer's" proteins and vice versa. Scientists are learning more about how and why this happens and what it means for symptoms and for disease progression. What can you do to prevent them? Live as healthfully as possible. For Parkinson's, regular exercise and a Mediterranean or MIND-type diet are associated with lower rates of diagnosis. Same goes for Alzheimer's. A recent report even indicated there are at least 14 modifiable risks for Alzheimer's, including vision and hearing loss. (https://shorturl.at/jRq29) The key is getting started earlier in life, as these diseases start in the brain and body decades before the symptoms come out and they are diagnosed.