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FIGURE 2 — Dysregulated Lipid Metabolism and Its Role in α-Synucleinopathy in Parkinson's D

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FIGURE 2 — Dysregulated Lipid Metabolism and Its Role in α-Synucleinopathy in Parkinson's D
FIGURE 2Figure 2
Schematic representation of the role of α-synuclein in lipid uptake and metabolism. α-syn deficiency inhibits the uptake of palmitic acid and arachidonic acid and their further metabolism into glycerophosphocholine, while there is an increase in the incorporation of docosahexaenoic acid into glycerophosphoethanolamine, glycerophosphoinositol, and glycerophosphoserine. The absence of α-syn also reduces levels of phosphatidylglycerol and cardiolipin in mitochondria. Mutant α-synuclein has been shown to enhance the activity of acyl-CoA synthetase and lead to an increased generation of triacylglycerols, while wild-type α-synuclein may inhibit phospholipase D2, which hydrolyzes glycerophospholipids into diacylglycerols and phosphatidic acid. DAG, diacylglycerol; FA, fatty acid; GPC, glycerophosphocholine; GPE, glycerophosphoethanolamine; GPI, glycerophosphoinositol; GPS, glycerophosphoserine; TAG, triacylglycerol.
PubMed: paper-1940e5ca5bb3
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pmidpaper-1940e5ca5bb3
captionSchematic representation of the role of α-synuclein in lipid uptake and metabolism. α-syn deficiency inhibits the uptake of palmitic acid and arachidonic acid and their further metabolism into glycero
image_urlhttps://www.ebi.ac.uk/europepmc/articles/PMC6470291/bin/fnins-13-00328-g002.jpg
paper_titleDysregulated Lipid Metabolism and Its Role in α-Synucleinopathy in Parkinson's Disease.
figure_labelFIGURE 2
figure_number2
_schema_version1
source_strategypmc_api
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