Neurochemical studies: an update on Alzheimer's disease.
A cascade of molecular and cellular events probably leads to the formation of the lesions that characterize Alzheimer's disease. The author reviews a representative selection of the extensive literature documenting protein abnormalities in Alzheimer's disease, using two broad categories of abnormality--changes in protein concentrations and changes in the molecular nature of proteins. The possible mechanisms of aberrations of the major proteins implicated in plaque and tangle formation--amyloid peptide precursor, tau, other microtubule-associated proteins, neurofilaments, and ubiquitin--are considered in neuritic plaque, the neurofibrillary tangle, other neuronal inclusions, and neurotransmission. The importance of a gene in the q21 band of chromosome 21 in familial Alzheimer's disease is discussed. The voluminous data on Alzheimer's disease raise intriguing possibilities about the key event in the pathogenesis of the disease, but further investigation is necessary to identify the event conclusively.
Davies
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Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461.
D000544:Alzheimer Disease / Q000473:pathology*; D001923:Brain Chemistry; D002891:Chromosomes, Human, Pair 21; D006801:Humans; D009454:Neurofibrils / Q000032:analysis; D011506:Proteins / Q000032:analysis*; D009435:Synaptic Transmission
D011506:Proteins