title: Beta-amyloid auto-antibodies are reduced in Alzheimer's disease.
abstract: Accumulation and cytotoxicity of amyloid beta (Aβ) are understood as the major cause of Alzheimer's disease (AD). There is evidence that naturally occurring antibodies against amyloid beta (Aβ) protein play a role in Aβ-clearance, and such a mechanism appears to be impaired in AD. In the present study, the anti-Aβ antibodies in the serum from individuals with and without late onset AD were measured using ELISA and dot-blot methods. Aβ auto-antibodies in serum were mainly targeted to Aβ1-15 epitope and its titer was significantly lower in AD patients than elderly non-AD controls (NC). The dot-blot analysis further demonstrated that auto-antibodies against fibrillar Aβ42, Aβ1-15 and Aβ16-30 epitopes were all in a lower level in AD than in NC. The isotypes of the auto-antibodies were mainly non-inflammatory IgG2 type. We also analyzed the relationship of auto-Aβ antibody levels with the genotypes of apolipoprotein E (ApoE) and ANKK1/DRD2 gene.
authors.affiliation: Center for Neuroscience and Regenerative Medicine, Department of Neurology, Uniformed Services University of the Health Sciences, Bethesda, MD, United States. Electronic address: bao-xi.qu.ctr@usuhs.edu.
authors.forename: Bao-Xi
authors.initials: BX
authors.lastname: Qu
authors.affiliation: Center for Neuroscience and Regenerative Medicine, Department of Neurology, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.
authors.forename: Yunhua
authors.initials: Y
authors.lastname: Gong
authors.affiliation: Center for Neuroscience and Regenerative Medicine, Department of Neurology, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.
authors.forename: Carol
authors.initials: C
authors.lastname: Moore
authors.affiliation: Department of Neurology, University Texas Southwestern Medical Center, Dallas, TX, United States.
authors.forename: Min
authors.initials: M
authors.lastname: Fu
authors.affiliation: Department of Psychiatry, University Texas Southwestern Medical Center, Dallas, TX, United States.
authors.forename: Dwight C
authors.initials: DC
authors.lastname: German
authors.affiliation: Department of Surgery, University Texas Southwestern Medical Center, Dallas, TX, United States.
authors.forename: Ling-Yu
authors.initials: LY
authors.lastname: Chang
authors.affiliation: Department of Neurology, University Texas Southwestern Medical Center, Dallas, TX, United States.
authors.forename: Roger
authors.initials: R
authors.lastname: Rosenberg
authors.affiliation: Center for Neuroscience and Regenerative Medicine, Department of Neurology, Uniformed Services University of the Health Sciences, Bethesda, MD, United States.
authors.forename: Ramon
authors.initials: R
authors.lastname: Diaz-Arrastia
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000235:genetics / Q000276:immunology*; D016229:Amyloid beta-Peptides / Q000276:immunology*; D001057:Apolipoproteins E / Q000235:genetics; D001323:Autoantibodies / Q000097:blood / Q000276:immunology*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005838:Genotype; D006801:Humans; D007107:Immune System / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000276:immunology*; D017346:Protein Serine-Threonine Kinases / Q000235:genetics; D017448:Receptors, Dopamine D2 / Q000235:genetics
chemical_list: D016229:Amyloid beta-Peptides; D001057:Apolipoproteins E; D001323:Autoantibodies; C581293:DRD2 protein, human; D010446:Peptide Fragments; D017448:Receptors, Dopamine D2; C480626:amyloid beta-protein (1-15); C075222:amyloid beta-protein (1-42); C489948:ANKK1 protein, human; D017346:Protein Serine-Threonine Kinases
keywords: ANKK1/DRD2; Alzheimer's disease; Amyloid beta antibodies; Apolipoprotein E (ApoE); Dot blot; ELISA