%0 Journal Article %T ELISA measurement of specific non-antigen-bound antibodies to A¦Â1-42 monomer and soluble oligomers in sera from Alzheimer's disease, mild cognitively impaired, and noncognitively impaired subjects %A Andrea C Klaver %A Mary P Coffey %A Lynnae M Smith %A David A Bennett %A John M Finke %A Loan Dang %A David A Loeffler %J Journal of Neuroinflammation %D 2011 %I BioMed Central %R 10.1186/1742-2094-8-93 %X Serum antibodies to A¦Â1-42 monomer and soluble oligomers in AD, MCI, and NCI subjects (10/group) were measured by ELISA, subtracting polyvalent antibody binding and dissociating antibody-antigen complexes. Differences in mean antibody levels were assessed for significance with repeated measures ANOVA using restricted maximum likelihood estimation, using Tukey-Kramer tests and confidence intervals for multiple comparisons. Spearman's rank correlation was used to determine associations between anti-monomer and anti-oligomer antibody concentrations. Estimated sample sizes required to detect effects of various sizes were calculated.There were no significant differences between groups for mean anti-A¦Â antibody levels, although these tended to be higher in AD than NCI specimens. Estimated group sizes of 328 and 150 for anti-A¦Â monomer and oligomer antibodies, respectively, would have been required for 80% power for significance at 0.05 for a 25% increase in the AD mean relative to the NCI mean. Serum antibody concentrations to A¦Â monomer and oligomers were strongly associated (correlations: 0.798 for undissociated sera, 0.564 for dissociated sera). Antibody-antigen dissociation significantly increased anti-A¦Â monomer but not anti-A¦Â oligomer antibody levels.The findings in this pilot study are consistent with relatively similar concentrations of specific, non-antigen-bound antibodies to A¦Â1-42 monomer and soluble oligomers in AD, MCI, and NCI sera. The differences between groups for these antibodies would have required approximate group sizes of 328 and 150, respectively, for a high probability for statistical significance. These findings do not support the hypothesis that reduced levels of anti-A¦Â antibodies might contribute to AD's pathogenesis.Amyloid-beta (A¦Â), the major plaque-associated protein in the Alzheimer's disease (AD) brain, has become the main target for AD therapy since the formulation of the "amyloid hypothesis" [1]. The significance of serum antibodies t %U http://www.jneuroinflammation.com/content/8/1/93