Beta-amyloid auto-antibodies are reduced in Alzheimer's disease

Bao Xi Qu, Yunhua Gong, Carol Moore, Min Fu, Dwight C. German, Ling Yu Chang, Roger Rosenberg, Ramon Diaz-Arrastia

Research output: Contribution to journalArticlepeer-review

34 Scopus citations


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. •ELISA and dot blot are applied to measure Aβ auto-antibodies in AD patients.•The auto-antibodies target Aβ1-15 and lower in AD than the control.•Low auto-antibodies are even more significant in AD patients over 65 years old.•Impairment of the immune system to Aβ could be one of the causes of AD.

Original languageEnglish (US)
Pages (from-to)168-173
Number of pages6
JournalJournal of Neuroimmunology
Issue number1-2
StatePublished - 2014


  • ANKK1/DRD2
  • Alzheimer's disease
  • Amyloid beta antibodies
  • Apolipoprotein E (ApoE)
  • Dot blot

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology


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