The pathogenesis of Alzheimer's disease.
Despite consensus on clinical and neuropathologic definitions of Alzheimer's disease, limited information is available on its causes and pathogenesis. Current data suggest interactions among the various possible biological and environmental influences that result in a common pathway leading to the disease. Biological influences include genetic mutations causing the disease phenotype and polymorphisms contributing to disease risk. Alterations in immune or inflammatory responses may also represent biological influences. Various environmental influences that may interact with endogenous biological factors include education, traumatic injury, oxidative stress, drugs, and hormone replacement. The author describes some recent findings that suggest possible pathogenic mechanisms, which may eventually have important treatment implications.
Department of Psychiatry and Biobehavioral Sciences, University of California at Los Angeles School of Medicine, and the Veterans Affairs Medical Center, USA.
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D000544:Alzheimer Disease / Q000209:etiology* / Q000235:genetics / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000502:physiology; D000818:Animals; D001057:Apolipoproteins E / Q000235:genetics / Q000502:physiology; D003866:Depressive Disorder / Q000453:epidemiology; D004522:Educational Status; D004967:Estrogens / Q000502:physiology; D005819:Genetic Markers; D005838:Genotype; D006801:Humans; D008565:Membrane Proteins / Q000502:physiology; D051379:Mice; D008822:Mice, Transgenic; D010641:Phenotype; D011110:Polymorphism, Genetic; D053764:Presenilin-1; D012307:Risk Factors
D016229:Amyloid beta-Peptides; D001057:Apolipoproteins E; D004967:Estrogens; D005819:Genetic Markers; D008565:Membrane Proteins; C508853:PSEN1 protein, human; D053764:Presenilin-1