The amyloid cascade hypothesis

The amyloid cascade hypothesis suggests that the accumulation of a protein called amyloid-beta in the brain is a central factor in the development of Alzheimer’s disease. This buildup forms sticky plaques that disrupt communication between brain cells, leading to inflammation and cell death. As these processes unfold, they may trigger further changes that contribute to the disease, including tau protein tangles. Essentially, the hypothesis links amyloid-beta accumulation to the broader range of symptoms and issues associated with Alzheimer’s, providing a framework for understanding the disease and guiding research toward potential treatments.