title: Inflammation, the complement system and the diseases of aging.
abstract: Inflammation is characteristic of neurodegenerative diseases of aging. Neuropathological evidence of activated microglia and activated astrocytes in lesioned areas, combined with epidemiological evidence of sparing of Alzheimer's disease (AD), Parkinson's disease (PD) and age-related macular degeneration (AMD) in long-term users of anti-inflammatory agents, indicates that inflammation is autodestructive of neurons. Locally produced autodestructive molecules include the membrane attack complex (MAC) of complement and oxygen-free radicals. Stimulation is provided by a variety of inflammatory cytokines. Agents which reduce the intensity of inflammation should have broad spectrum application in degenerative diseases of aging.
authors.affiliation: Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC, Canada.
authors.forename: Edith G
authors.initials: EG
authors.lastname: McGeer
authors.forename: Andis
authors.initials: A
authors.lastname: Klegeris
authors.forename: Patrick L
authors.initials: PL
authors.lastname: McGeer
mesh_terms: D000375:Aging / Q000502:physiology*; D000818:Animals; D003165:Complement System Proteins / Q000378:metabolism*; D006801:Humans; D007249:Inflammation / Q000378:metabolism*; D019636:Neurodegenerative Diseases / Q000145:classification / Q000378:metabolism* / Q000473:pathology; D009457:Neuroglia / Q000378:metabolism
chemical_list: D003165:Complement System Proteins