Polygenic pathways shape white matter vulnerability to Alzheimer’s disease-related pathophysiological changes
Background: The accumulation of amyloid-β1−42 (Aβ1−42) peptides and phosphorylated-Tau181 (p-Tau181) tangles from the preclinical stages of Alzheimer’s disease (AD) has led to a biological definition of the disease. However, among Aβ1−42-positive individuals, cognitive decline onset varies, and some never develop symptoms. Genetic influences on molecular pathways and their interactions with protei
