A hormone treatment contaminated with amyloid-β given to mice caused the protein’s accumulation in their brains, suggesting the same could have occurred in humans given the therapy.

A proposed definition of the disease emphasizes signs of neurodegeneration and the presence of β-amyloid and tau, rather than cognitive symptoms.

The test uses levels of plasma amyloid-β to estimate the buildup of protein plaques in the brain.

The once fringe idea is gaining traction among the scientific community.

Emerging evidence links bacterial or viral infection with the neuropathology of Alzheimer’s disease.

Examining the brains of seven patients who died of the prion disease called Creutzfeldt–Jakob, researchers find signs of Alzheimer’s pathology. 

Aggregate-forming amyloid β proteins are replenished more slowly with age, and this may contribute to a person's risk of developing Alzheimer’s disease.

An enzyme that cleaves tau protein in acidic cellular conditions may trigger early events in Alzheimer’s disease.