The molecular pathology of Alzheimer's disease

Abstract

Neurofibrillary pathology in Alzheimer's disease consists of paired helical filaments comprising tau protein. This pathology is correlated with dementia, but can appear in the first two decades of life. Extracellular amyloid β-protein arises through proteolytic processing of a transmembrane precursor, which involves the action of several enzymes. Mutations in the genes for the precursor and presenilin proteins accelerate the deposition of Aβ. Tau mutations cause other tauopathies in the absence of amyloid deposition, indicating that amyloid deposition is not a prerequisite for dementia. An improved understanding of Alzheimer's disease awaits to be obtained by molecular imaging of these pathologies.