The existing literature on the failures in AD clinical trials emphasized the urgent need to identify additional biomarkers involved in AD. Recent studies reported that autoantibodies are ubiquitous in human sera. However, it is unknown whether autoantibodies are upregulated in amyloid‐tau biomarkers‐confirmed AD. Researchers did this study to understand whether autoantibodies are upregulated in amyloid‐tau biomarker‐confirmed AD or not.
In total, the Forty subjects were enrolled in the study. They were people with mild dementia who were stratified into AD and non‐AD groups according to their cerebrospinal fluid levels of tau and Aβ42.
All controls and samples passed the quality control criteria to be in the study. The researchers, after initial screening, the researchers were further used for biomarker analysis. The researchers exclusively found Six autoantibodies with elevated responses to the following autoantigens in the AD group: nucleosome assembly protein 1‐like three and microtubule‐associated protein 4, pantothenic acid kinase 3, phosphoinositide‐3‐kinase regulatory subunit 1, protein tyrosine phosphatase type IVA member 1, and SRY box 15.
The study concluded through its findings that although some evidence identified autoantigens are linked to AD and cognitive dysfunction. The increased autoantibody levels were not reported in AD.