Decreased serum amyloid β1–42 autoantibody levels in Alzheimer’s disease, determined by a newly developed immuno-precipitation assay with radiolabeled amyloid β1–42 peptide

Background Autoantibodies against amyloid β (Aβ) peptide found in patients with Alzheimer’s disease (AD) also occur naturally in the general population independently of the cognitive status. Methods We compared serum Aβ1–42 autoantibody levels (Aβ1–42-AL) of 96 AD patients and 30 healthy elderly control subjects (HC), assessing their diagnostic value for AD with a newly developed immunoprecipitation assay with radiolabeled Aβ1–42 peptide. Results We found a highly significant decrease of Aβ1–42-AL in AD patients (p = .001) independently of age, cognitive status, and apolipoprotein Eε4 carrier status. Amyloid β1–42 autoantibody levels were correlated with gender in AD, with a higher level occurring in women. When Aβ1–42 autoantibody sensitivity (specificity) was set >80%, specificity (sensitivity) was below 50% to correctly allocate patients and healthy control subjects. Conclusions Our data indicate a potentially pathophysiologic decrease of serum Aβ1–42 antibodies in AD. Amyloid β1–42 antibodies in the serum alone, however, seem not to be useful as a diagnostic marker of AD.