Amyloid‐beta subspecies in individuals with Down Syndrome, sporadic Alzheimer's disease (sAD) and PS1 mutations ‐ comparison using IP‐Mass Spectrometry of plasma

Abstract

Background: Down Syndrome (DS) individuals develop Alzheimer's Disease (AD) neuropathology by the age of 40 due to the triplication of Chromosome 21 and the amyloid precursor protein gene. This genetic alteration leads to an overproduction of Aß, resulting in amyloid accumulation.