| Literature DB >> 25022335 |
Bao-Xi Qu1, Yunhua Gong2, Carol Moore2, Min Fu3, Dwight C German4, Ling-Yu Chang5, Roger Rosenberg3, Ramon Diaz-Arrastia2.
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. Published by Elsevier B.V.Entities:
Keywords: ANKK1/DRD2; Alzheimer's disease; Amyloid beta antibodies; Apolipoprotein E (ApoE); Dot blot; ELISA
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Year: 2014 PMID： 25022335 PMCID： PMC4410718 DOI： 10.1016/j.jneuroim.2014.06.017
Source DB: PubMed Journal: J Neuroimmunol ISSN： 0165-5728 Impact factor: 3.478