Abstract
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.
Highlights
The human antibody repertoire can be subdivided into conventional and naturally occurring antibodies, based on their originating B cell type
It is not surprising that many studies dealing with Naturally occurring autoantibodies (nAbs)-Aβ and nAbs-α-Syn titers in AD and Parkinson’s disease (PD) patients in comparison to control participants are available in the literature
For the development of reliable diagnostic markers and as therapeutic targets, the determination of nAbs-Aβ and nAbs-α-Syn titers are of certain interest in AD and PD research
Summary
The human antibody repertoire can be subdivided into conventional and naturally occurring antibodies, based on their originating B cell type. While conventional antibodies derive during life from plasma and memory B cells differentiated from B2 or marginal zone B cells after antigenic activation, naturally occurring antibodies arise in fetogenetic periods and are present from birth[1,2,3,4]. A fraction shows autoreactivity and is termed naturally occurring autoantibodies (nAbs), which are mostly from the IgM and IgA, fewer from the IgG type[7]. They circulate through human body fluids, maintain physiological homeostasis, support the clearance of distinct secreted proteins and apoptotic cells, and protect from pathologically altered structures like oxidatively damaged, aggregated, and non-functional lipids and proteins[8,9].
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