title: Immunotherapy for Alzheimer's disease.
abstract: Strong evidence exists indicating that chronic neuroinflammation contributes to the progression of Alzheimer's disease (AD). A major focus of AD-associated research has been amyloid-beta (Abeta) protein deposits. Vaccination with Abeta stimulates phagocytosis of Abeta in transgenic mouse models of AD, leading to clearance of the deposits. Similar vaccination in humans with AD has, however, led to meningoencephalitis in some cases. The difference probably depends on the initial level of brain inflammation, which is much higher in bona fide AD in humans than in the transgenic mice. Because both pro- and anti-inflammatory activation of immune cells are possible, stimulating the phagocytic action of microglia while simultaneously stimulating anti-inflammatory activity might be beneficial in AD.
authors.affiliation: Kinsmen Laboratory of Neurological Research at the University of British Columbia, Vancouver, BC V6T 1Z3, Canada. mcgeerpl@interchange.ubc.ca
authors.forename: Patrick L
authors.initials: PL
authors.lastname: McGeer
authors.forename: Edith
authors.initials: E
authors.lastname: McGeer
mesh_terms: D000544:Alzheimer Disease / Q000276:immunology* / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D000682:Amyloid / Q000378:metabolism; D016229:Amyloid beta-Peptides / Q000276:immunology* / Q000627:therapeutic use; D000818:Animals; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic; D010446:Peptide Fragments / Q000276:immunology* / Q000627:therapeutic use; D014611:Vaccination / Q000379:methods*
chemical_list: D000682:Amyloid; D016229:Amyloid beta-Peptides; D010446:Peptide Fragments; C075222:amyloid beta-protein (1-42)