All articles tagged with #beta amyloid
A Toronto-based research team proposes that Alzheimer's may be primarily an autoimmune disorder involving the brain's immune response, challenging the traditional view of beta-amyloid as the cause, and emphasizing the need for innovative treatment strategies beyond targeting amyloid plaques.
A new perspective suggests Alzheimer's may be an autoimmune disorder rather than solely a brain protein abnormality, emphasizing the immune system's role and calling for innovative research beyond the traditional beta-amyloid focus.
A new study suggests that the brain volume loss observed in Alzheimer's patients undergoing immunotherapy treatments may be due to the successful removal of beta-amyloid protein clumps, rather than tissue damage. Researchers from University College London found that this volume reduction correlates with the decrease in beta-amyloid levels, indicating that the shrinkage might be a positive sign of treatment efficacy. However, they caution that more research is needed to understand the long-term effects and potential risks of these treatments.
Emerging research suggests that Alzheimer's disease may be more of an immune system disorder than a traditional brain disease. This challenges the long-held belief that beta-amyloid protein accumulation is the primary cause of Alzheimer's. Researchers propose that beta-amyloid might play a protective role in the brain's immune system, but its inability to distinguish between harmful and healthy cells could lead to brain cell damage. This new perspective opens the possibility of treating Alzheimer's as an autoimmune disorder, focusing on immune-regulating pathways in the brain.
Recent research suggests that Alzheimer's disease may not primarily be a brain disease but rather an autoimmune disorder involving the brain's immune system. This theory posits that beta-amyloid, traditionally seen as a harmful protein, is actually part of the brain's immune response, which mistakenly attacks brain cells due to similarities with bacterial membranes. This new perspective challenges the long-held focus on beta-amyloid and calls for exploring alternative treatment pathways, as conventional autoimmune therapies may not be effective for Alzheimer's.
A new study published in Cell Reports Medicine challenges the traditional view that beta-amyloid plaques are the sole cause of Alzheimer's disease, identifying over 20 proteins that co-accumulate with beta-amyloid, including midkine and pleiotrophin, which may accelerate its aggregation. This discovery suggests a more complex interplay of proteins in Alzheimer's development, potentially leading to novel therapeutic strategies targeting multiple proteins. The findings could also impact the understanding and treatment of other amyloid-related neurodegenerative disorders.
The European Medicines Agency has approved Lecanemab, a drug targeting the cause of Alzheimer's disease, marking a potential turning point in its treatment. Developed by BioArctic and Eisai, Lecanemab aims to delay Alzheimer's progression by removing beta-amyloid plaques in the brain. While it offers hope, the drug's benefits are limited, delaying symptoms by about five months, and it poses risks like brain hemorrhages. The approval highlights the ongoing challenges and potential of antibody therapies in Alzheimer's treatment, with further research and infrastructure needed for widespread application.
A study by Mass General Brigham suggests that a maternal history of Alzheimer's disease may significantly impact a person's genetic risk of developing the condition, more so than paternal history. Researchers found that participants with a maternal history of memory issues had higher levels of beta-amyloid in their brains, a key biomarker for Alzheimer's. This finding highlights the importance of considering both maternal and paternal histories in assessing Alzheimer's risk and suggests that maternal inheritance may play a stronger role.
Researchers at The Buck Institute for Research in Aging have found that boosting mitochondrial health can delay the toxic effects of beta-amyloid proteins, which are associated with Alzheimer's disease. Using a worm model, they discovered that beta-amyloid and aging drive other proteins to become insoluble, contributing to the disease. By enhancing mitochondrial function with compounds like urolithin A, they were able to mitigate some of these effects, suggesting a potential new approach for Alzheimer's treatment.
A new report suggests that nose picking may increase the risk of developing Alzheimer's disease, as a protein called beta-amyloid, believed to be a cause of progressive dementia, may be produced in the brain as a defense mechanism to pathogens introduced via the nasal cavity. While nose picking isn't the sole cause of Alzheimer's, the report recommends frequent hand washing and the use of hand sanitizers as routine hygienic procedures to reduce the risk.
Quest Diagnostics has launched AD-Detect, the first direct-to-consumer blood test that detects abnormal levels of beta amyloid, a protein associated with Alzheimer's disease. Priced at $399, the test allows individuals aged 18 and older with mild memory loss or a family history of Alzheimer's to assess their risk for the disease. If the test is positive, users will be contacted by a doctor to discuss next steps. While the test has not undergone FDA review, it can be prescribed by a healthcare provider.
Groundbreaking Alzheimer's drugs that target beta amyloid may be less effective for Black Americans due to higher exclusion rates in clinical trials. Older Black Americans have twice the rate of dementia as their white peers, but were screened out of trials at a higher rate due to insufficient amyloid levels. Hispanics also faced higher exclusion rates. The disparity in beta amyloid raises questions about who will benefit from the new treatments. Some researchers are exploring whether Black patients experience dementia due to causes other than Alzheimer's or if the disease manifests differently in diverse populations. The low enrollment of diverse populations in clinical trials highlights the need for a better understanding of Alzheimer's in underrepresented groups.
Deep sleep, also known as non-REM slow-wave sleep, could help protect against memory loss in older adults with a high burden of Alzheimer’s disease, according to new research. The study found that deep sleep acts as a “cognitive reserve factor” that increases resilience against the beta-amyloid protein, which is associated with memory loss in dementia. The researchers believe that deep sleep may be an important factor in cognitive reserve, and improving sleep quality, even in older adults, could potentially help mitigate the impact of Alzheimer’s disease on memory.
Deep sleep, also known as non-REM slow-wave sleep, may help reduce memory loss in older adults facing a heightened burden of Alzheimer’s disease. Superior amounts of deep sleep can act as a protective factor against memory decline in those with existing high amounts of Alzheimer’s disease pathology, potentially helping to alleviate some of dementia’s most devastating outcomes. Disrupted sleep has previously been associated with faster accumulation of beta-amyloid protein in the brain, which is linked to memory loss caused by dementia.
Eli Lilly's experimental Alzheimer's drug, donanemab, has shown a 35% reduction in decline of thinking skills in people with early-stage Alzheimer's in an 18-month trial. The drug targets and clears away beta-amyloid, a sticky protein that builds up into brain-clogging plaques. However, the drug also comes with risks of brain side effects, which caused the deaths of three participants in the study. Lilly plans to release more details at an international Alzheimer's meeting this summer and is seeking FDA approval of the drug.