Alzheimer's disease

Acetylcholine levels generally begin a gradual decline around middle age and decline sharply in people with Alzheimer's disease.

Studies published between 1980 and 1996 reported that hormone therapies were associated with reduced risks of Alzheimer's disease, heart attack, and hip fracture.

Mutations in the presenilin 2 (PSEN2) gene are a rare inherited genetic cause that can virtually guarantee early-onset Alzheimer's disease.

Accumulation of tau protein in the brain is a hallmark pathological feature that is associated with the onset of cognitive decline in Alzheimer's disease.

Programmed cell death is a regulated cellular process that determines when cells end their lives and is essential for health; dysregulation of programmed cell death is implicated in diseases such as Alzheimer's disease (excessive neuronal death) and cancer (insufficient death of tumor cells).

Misfolded amyloid proteins can replicate and form crystal-like structures, and such amyloid aggregation is associated with neuron death in Alzheimer's disease.

Women are diagnosed with Alzheimer's disease nearly twice as often as men; proposed explanations for this sex difference include longer female life expectancy, hormonal changes such as shifts in estrogen during menopause, and differences in diagnostic patterns (for example, women being more likely to seek medical help for memory concerns).

The hippocampus and entorhinal cortex are among the first brain regions affected in Alzheimer's disease.

Amyloid-beta and tau are proteins linked to Alzheimer's disease, and elevated levels of these proteins can indicate early stages of Alzheimer's before clinical memory problems appear.

Epidemiological research indicates that increasing daily step counts from very low activity to several thousand steps per day is associated with slower cognitive decline and reduced accumulation of disease-related brain proteins among older adults at higher risk for Alzheimer's disease.

Amyloid proteins aggregate into extracellular plaques and tau proteins form intracellular tangles, and the combined presence of amyloid plaques and tau tangles disrupts neuronal communication and is associated with memory loss and cognitive decline in Alzheimer's disease.

The APOE ε4 genetic variant is associated with an increased risk of developing Alzheimer's disease.

Specialized brain imaging that measures amyloid burden can be used to quantify the biological severity of Alzheimer's-related pathology and can be expressed on a numerical scale to help estimate future risk of cognitive decline.