All articles tagged with #amyloid beta
Australian researchers in Griffith University show, in mice, that Chlamydia pneumoniae can travel from the nasal cavity to the brain via the olfactory and trigeminal nerves, with amyloid-beta deposits forming within days. Nasal epithelial injury increased bacterial load and brain involvement, but there are no human data yet and the causal role for Alzheimer's remains unproven; a human study is planned.
A Cedars-Sinai study shows Chlamydia pneumoniae can invade the retina and brain, triggering inflammation, nerve cell loss, and amyloid-beta buildup linked to Alzheimer's; higher bacterial levels correlate with worse cognition, especially in APOE4 carriers. The research suggests chronic infection and inflammation could drive Alzheimer's, and the retina might serve as a noninvasive window for early detection and new treatments targeting infection and inflammation.
In a study of 62 older adults, more non-REM deep sleep was linked to better memory performance even in people with Alzheimer’s-like brain changes, suggesting deep sleep may buffer against cognitive decline independent of education or activity. The findings highlight sleep quality as a potentially modifiable risk factor, though long-term studies are needed and sleeping pills may not offer the same benefit. Lifestyle tweaks to improve sleep—like avoiding late caffeine, exercising, limiting screens, and a warm pre-bed routine—could help preserve memory as we age.
Researchers identified two brain receptors (SST1 and SST4) that regulate neprilysin, the enzyme that degrades amyloid beta. Activating both receptors in mice raised neprilysin levels, reduced amyloid buildup, and improved memory-related behavior, suggesting a potential for safe, affordable oral Alzheimer’s treatments that enhance the brain’s own plaque-cleaning system; however, findings are preclinical and require human studies.
Researchers find that brief, rhythmic increases in CO2 (intermittent hypercapnia) can enhance glymphatic clearance and cerebrospinal fluid flow in both healthy individuals and people with Parkinson's, potentially aiding removal of brain toxins such as amyloid-beta; however, the durability of the effect and its impact on disease progression remain unclear.
A mouse study shows tumors releasing cystatin-C into the bloodstream can cross the blood-brain barrier, bind amyloid-beta, and activate microglia via Trem2 to clear plaques, sometimes improving memory in Alzheimer’s-like mice. While intriguing, these results are in animals and it's unknown whether humans would experience a similar protective effect; researchers are exploring therapies that mimic this mechanism without cancer.
A mouse study found that human tumors implanted in Alzheimer’s-model mice released cystatin-C into the bloodstream, which crossed the blood–brain barrier and bound to amyloid-beta plaques. This activated brain microglia via Trem2, boosting plaque clearance and sometimes improving memory. While intriguing as a potential pathway to treat or prevent Alzheimer’s, the findings are in mice and may not translate to humans, where cancer and Alzheimer's have a complex, inverse epidemiological relationship. Future work may explore therapies that mimic cystatin-C’s beneficial effects without cancer.
Researchers identify LilrB2 as a shared receptor that Reacts to amyloid beta and the inflammatory fragment C4d to trigger neurons to prune their own synapses, linking two major Alzheimer's theories. This neuron-autonomous mechanism suggests therapies should aim to protect synapses rather than solely dismantle plaques to preserve memory.
Scientists have discovered two brain receptors, SST1 and SST4, that regulate the breakdown of amyloid beta, a protein linked to Alzheimer's disease. Activating these receptors increases neprilysin levels, reduces amyloid plaques, and improves memory in models, suggesting a potential new, safer, and less expensive treatment approach compared to current antibody therapies.
A study in mice shows that increasing the protein Sox9 reactivates brain cells' cleanup functions, reducing Alzheimer's-like plaques and improving memory, suggesting a potential new treatment approach targeting brain maintenance cells called astrocytes.
A study in mice shows that increasing the protein Sox9 reactivates brain cells' cleaning functions, reducing Alzheimer's-like plaques and improving memory, suggesting a potential new treatment approach targeting brain maintenance cells called astrocytes.
A study published in Nature Medicine found that even modest increases in physical activity, such as walking 3,000-7,500 steps daily, can slow cognitive decline and tau protein buildup in older adults at risk for Alzheimer's, suggesting lifestyle changes may delay disease progression.
Recent research uncovers a harmful interaction between amyloid beta and fibrinogen that forms resistant blood clots, contributing to early signs of Alzheimer's disease by damaging blood vessels and synapses, and suggests targeting this complex could offer new therapeutic avenues.
Scientists have developed a novel nanoparticle-based approach that repairs the blood-brain barrier in mice, leading to rapid clearance of Alzheimer's-related plaques and improved cognitive function, suggesting a potential new direction for treatment research, though human applicability remains uncertain.
Scientists at St. Jude's have discovered that the protein midkine can prevent the formation of toxic amyloid beta clumps associated with Alzheimer's, suggesting potential new avenues for treatment.