Advances in the pathogenesis of Alzheimer’s disease: a re-evaluation of amyloid cascade hypothesis
1 Shanghai Engineering Research Center for Molecular Therapeutics and New Drug Development, East China Normal University, Shanghai, 200062, China
2 Institute of Chemical and Translational Genomics, East China Normal University, Shanghai, 200062, China
3 Key Laboratory of Brain Functional Genomics, Ministry of Education, Shanghai Key Laboratory of Brain Functional Genomics, East China Normal University, 3663 Zhongshan Road (N), Shanghai, 200062, China
Translational Neurodegeneration 2012, 1:18 doi:10.1186/2047-9158-1-18Published: 21 September 2012
Alzheimer’s disease (AD) is a common neurodegenerative disease characterized clinically by progressive deterioration of memory, and pathologically by histopathological changes including extracellular deposits of amyloid-beta (A-beta) peptides forming senile plaques (SP) and the intracellular neurofibrillary tangles (NFT) of hyperphosphorylated tau in the brain. This review focused on the new developments of amyloid cascade hypothesis with details on the production, metabolism and clearance of A-beta, and the key roles of some important A-beta-related genes in the pathological processes of AD. The most recent research advances in genetics, neuropathology and pathogenesis of the disease were also discussed.