Study reveals the role of the urea cycle in the brain and explores the dual nature of astrocytes in the brains of those with Alzheimer's pathology.
A smaller version of the amyloid-beta protein, AB 1-40, builds up on the wall of small arteries and reduces blood flow to the brain, a new study reports.
Rapamycin, a drug approved for the treatment of cancer and transplant patients increases amyloid-beta protein plaques in the brains of mice.
The heat produced by amyloid-beta aggregation may cause other, healthy amyloid-beta to aggregate, causing more and more aggregates to form. However, with the addition of a novel drug compound, amyloid-beta aggregation can be stopped and the cell temperature lowered.
A new mouse study reveals a breakdown in the process that clears brain cells of waste products precedes the buildup of amyloid plaques associated with Alzheimer's disease.
A combination of patient-reported subjective cognitive impairment and measurable clinical symptoms, such as amyloid-beta accumulation in the cerebrospinal fluid, may help in the early diagnosis of Alzheimer's disease.
The corn-derived MetO-rich protein, when injected, prompts the immune system to produce antibodies against the MetO component of amyloid beta. Older mice injected with the MetO-rich protein showed 50% improvement in memory compared to the control animals. The findings could be key to the development of a potential vaccine for Alzheimer's.
The accumulation of amyloid-beta and tau proteins disrupts the connections between brain regions associated with memory years before symptoms of Alzheimer's disease appear.
Measuring blood levels of P-tau181 may allow doctors to diagnose Alzheimer's before the onset of symptoms. Elevated levels of P-tau181 in the blood were associated with greater amyloid beta accumulation in the brain and outperformed two other biomarkers in predicting signs of amyloid beta in brain scans.
Like cognitive deficits, psychiatric symptoms such as depression, apathy, and anxiety associated with Alzheimer's disease appear to be a direct consequence of underlying brain changes as a result of increased amyloid-beta accumulation.
3,6’-dithiopomalidomide (DP), an anti-inflammatory drug candidate, protected mouse models of Alzheimer's disease against cognitive decline by reducing neuroinflammation.