The genetics and molecular pathology of Alzheimer's disease: roles of amyloid and the presenilins.
The study of Alzheimer's disease (AD) has had more than its share of controversy. In the last few years, however, considerable consensus has been developed that certain molecular events in the brain occur many years or decades before clinical symptoms, and a rough outline of the pathogenic cascade has emerged from the studies of many investigators. Progress in two broad areas has led to this consensus: molecular genetics and biochemical pathology. In this article, the exciting new understanding of the pathogenesis of AD is reviewed and its affect on the patient population is discussed.
Selkoe
D J
DJ
Department of Neurology and Neuroscience, Harvard Medical School, Center for Neurologic Diseases, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA. selkoe@cnd.bwh.harvard.edu
D000368:Aged; D000544:Alzheimer Disease / Q000175:diagnosis / Q000235:genetics* / Q000473:pathology; D000682:Amyloid / Q000235:genetics*; D001921:Brain / Q000473:pathology; D015870:Gene Expression / Q000502:physiology; D005819:Genetic Markers / Q000235:genetics; D020022:Genetic Predisposition to Disease / Q000235:genetics; D006801:Humans; D008565:Membrane Proteins / Q000235:genetics*; D053764:Presenilin-1; D053766:Presenilin-2
D000682:Amyloid; D005819:Genetic Markers; D008565:Membrane Proteins; C508853:PSEN1 protein, human; C508861:PSEN2 protein, human; D053764:Presenilin-1; D053766:Presenilin-2