New Insights into the Molecular Bases of Familial Alzheimer's Disease.

ABSTRACT: Like several neurodegenerative disorders, such as Prion and Parkinson diseases, Alzheimer's disease (AD) is characterized by spreading mechanism of aggregated proteins in the brain in a typical "prion-like" manner. Recent genetic studies have identified in four genes associated with inherited AD (amyloid precursor protein-APP, Presenilin-1, Presenilin-2 and Apolipoprotein E), rare mutations which cause dysregulation of APP processing and alterations of folding of the derived amyloid beta peptide (A). Accumulation and aggregation of A in the brain can trigger a series of intracellular events, including hyperphosphorylation of tau protein, leading to the pathological features of AD. However, mutations in these four genes account for a small of the total genetic risk for familial AD (FAD).

SUBMITTER: D'Argenio V 

PROVIDER: S-EPMC7354425 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature