title: Interleukin-1, neuroinflammation, and Alzheimer's disease.
abstract: Interleukin-1 (IL-1)-1) is a pluripotent immunomodulatory cytokine that has an initiating role in cellular and humoral immunity in the periphery. Il-1 is overexpressed in Alzheimer brain, and this overexpression is directly related to plaque formation and progression, nonsensical growth of dystrophic neurites, and neuronal overexpression of acetylcholinesterase. IL-1 has a number of actions relevant to Alzheimer's disease, including excessive expression of neuronal Abeta precursor protein and other plaque-associated proteins, and induction of astrocyte activation and astrocytic overexpression of S100B. These latter events may be related to the overgrowth of dystrophic neurites in neuritic plaques, a necessary event for conversion of diffuse Abeta deposits into the neuritic amyloid plaques diagnostic of Alzheimer's disease. Four new genetic studies underscore the relevance of IL-1 to Alzheimer pathogenesis, showing that homozygosity of a specific polymorphism in the IL-1A gene at least triples Alzheimer risk, especially for an earlier age of onset and in combination with homozygosity for another polymorphism in the IL-1B gene.
authors.affiliation: Department of Pathology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA. mrakroberte@uams.edu
authors.forename: R E
authors.initials: RE
authors.lastname: Mrak
authors.forename: W S
authors.initials: WS
authors.lastname: Griffin
mesh_terms: D000544:Alzheimer Disease / Q000235:genetics / Q000473:pathology*; D000818:Animals; D001923:Brain Chemistry / Q000235:genetics / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000235:genetics / Q000473:pathology*; D007375:Interleukin-1 / Q000235:genetics / Q000502:physiology*; D009474:Neurons / Q000473:pathology*; D011110:Polymorphism, Genetic / Q000235:genetics
chemical_list: D007375:Interleukin-1