Description
Title: GM1 Ganglioside’s Crucial Function in Parkinson’s Disease
Abstract: In this review, we have made an effort to condense our findings, which demonstrate a systemic ganglioside GM1 deficiency in the tissues of Parkinson’s disease (PD). These include peripheral nervous system organs like the colon and the heart as well as neuronal tissues that are well known to play a role in Parkinson’s disease, such as the substantia nigra of the brain. Additionally, we studied peripheral blood mononuclear cells, skin, and fibroblasts, which are tissues not directly connected to neuronal signaling. We present similar results for the metabolic precursor to GM1 known as ganglioside GD1a. We go over the most likely reasons for these GM1 deficiency symptoms and the ensuing biochemical mechanisms that underlie the loss of neuronal viability and typical function. A mouse PD model that involves partial GM1 deficiency caused by mono-allelic disruption of the B4galnt1 gene offers compelling evidence in favor of this theory. We draw attention to the fact that both the brain and the periphery experience progressive loss of GM1/GD1a, eliminating the need to hypothesize the transfer of PD symptoms between these tissues. The implications of these findings for a potential disease-modifying therapy for PD:GM1 replacement, which is strongly implicated in animal studies and clinical trials, are discussed in the final section.
Keywords: Parkinson’s disease; GM1; ganglioside; multi-system disorder; neuroprotection
Paper Quality: SCOPUS / Web of Science Level Research Paper
Subject: Biomolecules
Writer Experience: 20+ Years
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