Strategies for Immunization and Neurodegeneration Prevention

According to the most recent science, Amyloid is the Match. Neuroinflammation is the Wildfire. Alzheimer’s doesn’t start with memory loss. It starts decades earlier when amyloid plaques begin accumulating in the brain. But here’s the real problem: Amyloid alone isn’t enough to cause widespread damage. The real destruction happens when neuroinflammation turns that small spark into a raging fire. So what can we do? Prevention is our most powerful, evidence-based tool. The key is to stop the match from striking and control the fire before it spreads. Clear the match—prevent amyloid buildup: ✔️ Prioritize deep sleep—your brain’s nightly cleaning crew. ✔️Eat an anti-inflammatory diet (MIND/Mediterranean/Anti-Inflammatory). ✔️ Move daily—exercise helps remove toxic proteins. Control the wildfire—reduce neuroinflammation: ✔️ Heal your gut-brain connection—diverse microbiomes = less inflammation. ✔️ Keep blood sugar stable—Alzheimer’s is often called "Type 3 diabetes." ✔️ Manage chronic stress—cortisol fuels inflammation. The takeaway? You have more control than you think. Prevention starts NOW. What’s one habit you practice to support brain health? Let’s share strategies! #BrainHealth #Neuroinflammation #AlzheimersPrevention #AgelessAging #CognitiveHealth #HealthyAging

Prototype #mRNA vaccine for Alzheimer's Disease (AD). Specifically, mRNA encodes 3 copies of the N-terminal region of human Aβ spanning amino acids 1–11 attached to highly immunogenic epitopes. A preventive AD vaccine developed through this strategy could stimulate long-lasting antibodies in individuals at risk of AD, potentially inhibiting the aggregation/accumulation of pathological Aβ and tau proteins and delaying the onset of dementia.  

Rethinking Alzheimer’s Disease: From Plaques to the Inflammasome A growing body of evidence is reshaping how we understand Alzheimer’s disease (AD). Beyond amyloid plaques and tau tangles, research is now spotlighting the innate immune system, specifically the NLRP3 inflammasome, as a critical driver of neurodegeneration. A new study in the Journal of Alzheimer’s Disease characterizes AD as an autoinflammatory immune pathology, highlighting: Activation of the NLRP3 inflammasome in response to amyloid-β and phosphorylated tau Upregulation of proinflammatory cytokines and immune-related secretomes Evidence for trained immunity and even cell trans-differentiation, where brain cells adopt inflammatory immune phenotypes At Halia Therapeutics, we’re pioneering treatments that directly target these underlying inflammatory pathways. Our lead candidate, HT-4253, is an oral LRRK2 inhibitor designed to suppress neuroinflammation in APOE4 homozygous individuals—those at highest genetic risk for AD. Inflammation is not just a symptom of Alzheimer’s—it may be the starting point. It’s time to rethink how we treat neurodegeneration. If we can intercept the cycle of inflammation and immune dysfunction early, we may not only slow progression but also prevent disease onset. Let’s move beyond plaque and start targeting what’s upstream! https://lnkd.in/gXkK6_pi #AlzheimersDisease #Neuroinflammation #Inflammasome #TrainedImmunity #HaliaTherapeutics #Neuroscience #PrecisionMedicine #Biotech