All articles tagged with #amyloid plaques
A 79-year-old Pompano Beach man with Alzheimer's completed 18 months of Kisunla infusions to target amyloid plaques, and a final PET scan showed the plaques had cleared. Doctors say the anti-amyloid therapy slows cognitive decline but is not a cure, and Broward Health North's Memory Disorder & Alzheimer's Center is treating more than 60 patients with Kisunla.
A Baylor College of Medicine study shows boosting Sox9 in aging astrocytes increases MEGF10-mediated phagocytosis, leading to clear amyloid plaques and preserved cognition in Alzheimer's-model mice for six months; when Sox9 is knocked down, plaques accumulate faster and memory worsens, suggesting astrocyte-driven clearance as a potential therapy—yet human applicability remains unproven.
Researchers in a mouse model of Alzheimer's found microglia drive sleep loss; depleting most brain immune cells restored over two hours of nightly sleep and longer restorative sleep, even though amyloid plaques did not decrease, indicating microglial overactivity as a reversible sleep‑disruption driver. The work also points to portable EEG as a potential biomarker and explores repurposing existing drugs to calm microglia as possible therapies.
Researchers increased Sox9 to heighten astrocyte activity in mouse models of Alzheimer's, promoting the clearance of amyloid plaques and preserving cognitive function, suggesting a therapy that harnesses the brain’s own support cells to slow dementia progression.
Researchers at Indiana University identified neuronal IDOL as a new drug target for Alzheimer’s, showing that reducing IDOL activity in brain neurons lowers amyloid plaques and APOE levels, while boosting receptors that regulate APOE and amyloid. The neuron-focused approach produced stronger effects than targeting microglia, suggesting a potential multi-benefit therapy. Next steps include preclinical safety testing and evaluating whether IDOL blockade preserves synapses and reduces tau pathology.
A mouse study suggests the bodybuilding supplement HMB may slow Alzheimer’s-related changes by reducing amyloid plaques and neurofibrillary tangles and boosting neurotrophic factors, potentially supporting memory, but findings are preliminary and not yet proven in humans.
A Cell study (15 years in the making) finds that a protein called cystatin C, produced by cancer cells, can cross the blood–brain barrier and help break apart amyloid plaques in mouse models of Alzheimer’s disease, offering a possible explanation for the observed link between cancer and lower Alzheimer’s risk and suggesting a new avenue for drug development—though the findings are preclinical and in animals.
A study in mice shows that blood from young animals has protective effects against Alzheimer's disease by reducing amyloid plaque buildup and cognitive decline, while aged blood accelerates disease progression, highlighting the potential of targeting blood-borne factors for therapy.
Research indicates that getting more deep sleep, particularly NREM slow-wave sleep, may help protect memory and delay Alzheimer's progression in older adults, especially those with amyloid deposits, by supporting brain cleanup processes and memory consolidation.
Recent studies suggest that COVID-19 may cause lasting brain inflammation, increasing the risk of Alzheimer's disease by promoting cytokine production and amyloid plaque buildup, especially in susceptible populations.
A study from Washington University in St. Louis has found a strong link between visceral fat and Alzheimer's disease, suggesting that deep belly fat could predict Alzheimer's risk decades before symptoms appear. Unlike subcutaneous fat, visceral fat is associated with amyloid plaques in the brain, a hallmark of Alzheimer's. The research indicates that fat distribution, rather than BMI alone, may be a more reliable predictor of Alzheimer's risk. Additionally, the study highlights the role of cholesterol and insulin levels in Alzheimer's development, emphasizing the complex relationship between metabolic health and brain function.
New research indicates that brain volume loss observed in Alzheimer's patients undergoing immunotherapy, such as with lecanemab, is due to the removal of amyloid plaques rather than neuronal damage. This phenomenon, termed "amyloid-removal-related pseudo-atrophy" (ARPA), suggests that volume changes are a sign of treatment effectiveness and not harmful. The study, published in Lancet Neurology, emphasizes the need for better reporting and understanding of these changes as such therapies become more common.
Researchers at Mount Sinai have discovered a potential new method to treat Alzheimer's by targeting the plexin-B1 protein to improve plaque clearance in the brain. This breakthrough could slow or halt disease progression and opens new avenues for therapeutic strategies. The study emphasizes the role of reactive astrocytes and validates gene network models, marking a significant advance in Alzheimer's research.
Researchers at Mount Sinai Hospital have discovered that targeting the plexin-B1 protein can enhance the brain's ability to clear amyloid plaques, potentially slowing or halting Alzheimer's progression. This breakthrough emphasizes the role of reactive astrocytes and cellular interactions in developing new treatments for Alzheimer's disease.
Researchers are investigating whether a discontinued medical procedure used on children with growth-related disorders may have transmitted amyloid plaques, leading to the development of Alzheimer's disease in some patients. The study suggests that under certain circumstances, Alzheimer's could be transmitted from one person to another, similar to past cases of Creutzfeldt–Jakob disease transmission. While there is no evidence that Alzheimer's can be casually transmitted between individuals, the findings emphasize the need to review measures to prevent accidental transmissions via other medical and surgical procedures. Further research is needed to understand how contamination with amyloid proteins could progress to disease, and to explore the possibility of iatrogenic transmission of Alzheimer's disease through other means.