Inflammation and neurodegenerative diseases.
The decline in mental fitness associated with Alzheimer disease is accompanied by physical changes in the brain, including the development of characteristic plaques and neurofibrillary tangles, but the pathogenesis of those changes is not clear. Recent work suggests that the activation of microglia in response to injury, illness, aging, or other causes begins a cascade of events that can best be characterized as an inflammatory process. This cascade is mediated at first by the proinflammatory cytokine interleukin 1, which is overexpressed by the activated microglia. Through various pathways, interleukin 1 causes neuronal death, which activates more microglia, which in turn release more interleukin 1 in a self-sustaining and self-amplifying fashion. Over a period of years, this slow, smoldering inflammation in the brain destroys sufficient neurons to cause the clinical signs of Alzheimer disease.
Donald W Reynolds Department of Geriatrics, The University of Arkansas for Medical Sciences, and the Geriatric Research Education Clinical Center, Central Arkansas Veterans Healthcare System, Little Rock, AR 72205, USA. griffinsuet@uams.edu
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D000368:Aged; D000375:Aging / Q000276:immunology / Q000502:physiology*; D000544:Alzheimer Disease / Q000235:genetics / Q000276:immunology; D001921:Brain / Q000276:immunology* / Q000473:pathology; D004314:Down Syndrome / Q000150:complications / Q000276:immunology; D006801:Humans; D007249:Inflammation / Q000235:genetics / Q000276:immunology*; D007375:Interleukin-1 / Q000235:genetics / Q000276:immunology; D017628:Microglia / Q000276:immunology*; D009414:Nerve Growth Factors / Q000502:physiology; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins / Q000502:physiology
D007375:Interleukin-1; D009414:Nerve Growth Factors; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins