Description
Title: A relevant pathomechanism in synucleinopathies is lipotoxicity downstream of -Synuclein Imbalance.
Abstract: The abundant neuronal protein -synuclein (S) has been conclusively linked to the loss of neurons in Parkinson’s disease and other related brain diseases. However, we have learned surprisingly little about the precise mechanism by which S causes toxicity in these illnesses. Proteotoxicity, abnormal vesicle trafficking, mitochondrial dysfunction, and other toxicity theories have been put forth, and it appears likely that a variety of different mechanisms may work in concert to cause pathology. S-related lipotoxicity is a toxicity mechanism that has received more attention in recent years. When the metabolic needs for fatty acids are exceeded in a cell, a flux into dangerous non-oxidative metabolic pathways occurs, which is when biotoxicity typically occurs. A significant overlap between synucleinopathies and lipid storage disorders, most notably Gaucher’s disease, has been found using genetic and experimental methods. A growing body of research shows that lipid aberrations can cause synuclein misfolding as well as excess and incorrect folding of S. Does that imply that lipotoxicity, the buildup of harmful lipid species, or a change in lipid equilibrium are the main issues with synucleinopathies? Here, in an effort to get closer to an answer, we review the body of previous research.
Keywords: alpha-synuclein; lipids; lipidopathy; Parkinson’s disease; Lewy body dementia; neurotoxicity; stearoyl-CoA desaturase
Paper Quality: SCOPUS / Web of Science Level Research Paper
Subject: Biomolecules
Writer Experience: 20+ Years
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