All articles tagged with #amyloid plaques
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.
Researchers are exploring the use of CRISPR gene editing to develop new treatments for Alzheimer's disease caused by genetic mutations. While current treatments for Alzheimer's can slow the progression of the disease, they often do not benefit those in later stages or with specific genetic variants. CRISPR therapies have the potential to be a one-time cure, but there are challenges in applying this technology to the complex condition of Alzheimer's. Studies have shown promising results in mice, targeting genes such as APOE and PSEN1, but further research and clinical trials are needed to ensure safety and efficacy. Researchers hope that one day CRISPR gene editing could be combined with other therapies to provide personalized treatments for Alzheimer's patients.
Recent developments in Alzheimer's research, including the successful clinical trials of drugs like lecanemab and donanemab, have been hailed as a "game changer" in the field. These drugs, while not cures, have shown promise in slowing the progression of the disease and reducing cognitive decline in early-stage patients. Additionally, the development of diagnostic blood tests that can identify Alzheimer's-associated proteins may allow for early detection and treatment before major damage occurs. While there are concerns about the influence of Big Pharma and the challenges of implementing widespread prevention strategies, these advancements offer hope for managing Alzheimer's as a chronic condition rather than a terminal disease.
A study from the University of Kentucky suggests that certain anti-inflammatory drugs targeting the p38 protein may be effective treatments for Alzheimer's disease (AD). By suppressing the production of p38 in brain immune cells, researchers observed a decrease in the concentration of these cells around amyloid plaques, a key component of AD pathology. The study indicates that long-term suppression of p38 may not cause noticeable side effects and early inhibition could potentially alter the course of AD. However, further research is needed to determine the optimal timing for administering p38 inhibitors and the potential long-term effects of their suppression.
The U.S. Food and Drug Administration (FDA) has converted Leqembi (lecanemab-irmb), a treatment for Alzheimer's Disease, from accelerated approval to traditional approval after a confirmatory trial verified its clinical benefit. Leqembi is the first amyloid beta-directed antibody to receive traditional approval for Alzheimer's disease. The drug works by reducing amyloid plaques in the brain, a key characteristic of the disease. Alzheimer's disease affects over 6.5 million Americans and causes memory loss and cognitive decline. Leqembi demonstrated a significant reduction in decline compared to placebo in a Phase 3 clinical trial. The most common side effects of Leqembi include headache, infusion-related reactions, and amyloid-related imaging abnormalities.
The US Food and Drug Administration (FDA) has granted full approval to the Alzheimer's drug Leqembi, making it the first medication to slow the progression of the disease. The Centers for Medicare and Medicaid Services (CMS) will expand coverage of the drug, providing access to an estimated one million people with early forms of Alzheimer's. Leqembi, developed by Eisai and Biogen, received accelerated approval in January but faced limited use due to coverage restrictions. The drug, which costs $26,500 annually, was shown to slow cognitive decline by 27% in an 18-month clinical trial. However, it comes with side effects and requires regular brain imaging monitoring.