A Quantitative View on Naturally Occurring Autoantibodies in Neurodegenerative Diseases

Accumulation and aggregation of Beta-Amyloid (Aβ) and Alpha-Synuclein (α-Syn) are considered as central or even causative for the development of Alzheimer’s (AD) and Parkinson’s disease (PD). Therefore, the regulation of these proteins seems to be an essential aspect for prevention and is of central interest in current research aiming to find therapeutic approaches. The human immunological repertoire already contains such a regulatory system. Naturally occurring autoantibodies (nAbs) against the proteins Aβ (nAbs-Aβ) and α-Syn (nAbs-α-Syn) are part of the innate immune system and modulate the metabolism of their specific antigens including protein clearance and inhibition of aggregation. Thus, many researchers hypothesize that in the course of AD and PD, quantitative alterations of nAbs-Aβ and nAbs-α-Syn arise resulting in impaired proteastasis. Such alterations would represent promising, reliable biomarkers and indicate potential approaches for therapeutic strategies. Hence, it is not surprising that many studies dealing with nAbs-Aβ and nAbs-α-Syn titers in AD and PD patients in comparison to control participants are available in the literature. In this mini review, we summarize the current evidence. Furthermore, we critically discuss problems and future requirements for nAbs quantification when a clinical application is the overriding goal.