Phenotypic and neuropathological heterogeneity in autosomal dominant familial Alzheimer's disease, and implications for amyloid‐immunotherapy

Abstract

Background: In autosomal dominant Alzheimer's disease (ADAD), mutations in APP , PSEN1 and PSEN2 alter amyloid‐β processing, driving production of longer, aggregation‐prone amyloid‐β petides that deposit in parenchyma as plaques and blood vessel walls as cerebral amyloid angiopathy (CAA).

The paper