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FIGURE 1 — Dysregulated Lipid Metabolism and Its Role in α-Synucleinopathy in Parkinson's D
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Created: 2026-04-21T18:29:40
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FIGURE 1Figure 1
Lipid involvement in the aggregation and propagation of α-synuclein. Upon accumulation of unfolded α-syn, the monomers interact to form dimers, which can further grow to oligomers. These processes can take place both in the cytoplasm and in association with different cellular membranes. When soluble monomers continue to attach to oligomers, this eventually gives rise to amyloid fibrils, which can accumulate and form proteinaceous inclusions called Lewy bodies. α-Syn accumulation, oligomerization, and fibrillogenesis is highly affected by the lipid composition of the membranes it binds to, with a number of lipid species enhancing various steps of the process, as indicated on the diagram. The α-synuclein oligomers and fibrils formed are highly cytotoxic, leading to neurodegeneration. Cardiolipin is able to pull α-syn monomers from oligomeric fibrils, thereby buffering the toxicity. DHA, docosahexaenoic acid; GM1 and GM3, gangliosides; GPE, glycerophosphoethanolamine; GPI, glycerophosphoi
▸Metadata
| pmid | paper-1940e5ca5bb3 |
| caption | Lipid involvement in the aggregation and propagation of α-synuclein. Upon accumulation of unfolded α-syn, the monomers interact to form dimers, which can further grow to oligomers. These processes can |
| image_url | https://www.ebi.ac.uk/europepmc/articles/PMC6470291/bin/fnins-13-00328-g001.jpg |
| paper_title | Dysregulated Lipid Metabolism and Its Role in α-Synucleinopathy in Parkinson's Disease. |
| figure_label | FIGURE 1 |
| figure_number | 1 |
| _schema_version | 1 |
| source_strategy | pmc_api |
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