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.
Even for older people experiencing no general memory or thinking problems, performing poorly on a simple memory test may be linked to biomarkers for Alzheimer's disease.
Heart disease that causes brain dysfunction can lead to the development of Alzheimer's disease and triples the amount of amyloid-beta in the brain.