A SIGNALING PARALLEL BETWEEN SARS-CoV-2 SPIKE PROTEIN ANTIBODIES AND α-SYN FIBRILS: THE INDUCTION OF MULTIPLE SYSTEM ATROPHY AND AN EXPLANATION FOR THE DEMYLENATION SYMPTOMS OBSERVED IN COVID AND LONG COVID
September 17, 2021
A mechanism for the induction of Multiple System Atrophy may have been discovered. The molecular mimicry of spike protein antibodies is alarming (see image). Among the tissues that the spike protein antibodies interact with is Alpha Myelin. They also interact with FcγRIIB receptors. These receptors are what dampen, and in some cases completely turn off, the interferon response to SARS-CoV-2. It is thought this may be one of the main mechanisms of severe disease.
Interaction with FcγRIIB receptors may also be the mechanism for induction of Multiple System Atrophy and other Lewy Body diseases. What is most interesting is that α-syn fibrils also bind to FcγRIIB receptors and their downstream signaling causes cell-to-cell transmission of α-Syn.
What does this mean for neurodegeneration? I believe it is very likely the demyelination we are observing stems from this activation of FcγRIIB as it has been shown that α-Synuclein-induced myelination deficit is a cause of Multiple System Atrophy.
α-Synuclein-induced myelination deficit defines a novel interventional target for multiple system atroph
Prion-like Propagation of α-Synuclein Is Regulated by the FcγRIIB-SHP-1/2 Signaling Pathway in Neurons
SHP‐1 suppresses the antiviral innate immune response by targeting TRAF3
The Human FcγRII (CD32) Family of Leukocyte FcR in Health and Disease