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Amyloid precursor protein, presenilins, and alpha-synuclein: molecular pathogenesis and pharmacological applications in Alzheimer s disease Suh YH; Checler FPharmacol Rev 2002[Sep]; 54 (3): 469-525Alzheimer's disease (AD) is the most common cause of dementia that arises on a neuropathological background of amyloid plaques containing beta-amyloid (A beta) derived from amyloid precursor protein (APP) and tau-rich neurofibrillary tangles. To date, the cause and progression of both familial and sporadic AD have not been fully elucidated. The autosomal-dominant inherited forms of early-onset Alzheimer's disease are caused by mutations in the genes encoding APP, presenilin-1 (chromosome 14), and presenilin-2 (chromosome 1). APP is processed by several different proteases such as secretases and/or caspases to yield A beta and carboxyl-terminal fragments, which have been implicated in the pathogenesis of Alzheimer's disease. Alzheimer's disease and Parkinson's disease are associated with the cerebral accumulation of A beta and alpha-synuclein, respectively. Some patients have clinical and pathological features of both diseases, raising the possibility of overlapping pathogenic pathways. Recent studies have strongly suggested the possible pathogenic interactions between A beta, presenilins, and/or alpha-synuclein. Therefore, treatments that block the accumulation of A beta and alpha-synuclein might benefit a broad spectrum of neurodegenerative disorders. This review covers the trafficking and processing of APP, amyloid cascade hypothesis in AD pathogenesis, physiological and pathological roles of presenilins, molecular characteristics of alpha-synuclein, their interactions, and therapeutic strategies for AD.|Alzheimer Disease/drug therapy/metabolism/*pathology[MESH]|Amyloid beta-Protein Precursor/genetics/*metabolism[MESH]|Animals[MESH]|Disease Models, Animal[MESH]|Humans[MESH]|Membrane Proteins/genetics/*metabolism[MESH]|Mice[MESH]|Mice, Transgenic[MESH]|Nerve Tissue Proteins/genetics/*metabolism[MESH]|Presenilin-1[MESH]|Presenilin-2[MESH]|Protein Transport[MESH]|Synucleins[MESH]|alpha-Synuclein[MESH] |
