Molecular neuropathology of Alzheimer dementia and therapeutic approaches.

Abstract

Alzheimer’s disease (AD) is a neurodegenerative disorder of the central nervous system characterized by progressive loss of neurons in limbic and association cortices affecting almost all cognitive functions and memory. Additional neuropathological hallmarks of AD brains include large numbers of amyloid plaques (APs) containing fibers of Aβ peptides and neurofibrillary tangles (NFTs) consisting of overphosphorylated tau protein. Sporadic AD (SAD) is the most common form of dementia and accounts for more than 90 % of all cases. The etiology of SAD is complex and may be driven by both environmental and genetic factors. Presence of ApoE4 allele is the most important genetic risk factor for SAD although in the last 5 years additional genes were identified with smaller effects on the disorder. Several theories have been developed to explain the molecular basis of AD but none of these seems to offer a satisfactory explanation for the neurodegenerative phenotype of the disorder.