ArticleInternational journal of molecular sciences2021
Inhibition of Ceramide Synthesis Reduces α-Synuclein Proteinopathy in a Cellular Model of Parkinson's Disease.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- Lipid Metabolic Dysregulation Driven by OSMR Mutations Underlies Amyloidogenesis in Primary Localized Cutaneous Amyloidosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The role of lipid metabolism in neuronal senescence.FEBS open bio · 2026Review
- Inhibition of de novo ceramide synthesis mitigates alpha-synuclein pathology in a Parkinson's disease mouse model.NPJ Parkinson's disease · 2026Article
- Direct Current Stimulation (DCS) Modulates Lipid Metabolism and Intercellular Vesicular Trafficking in SHSY-5Y Cell Line: Implications for Parkinson's Disease.Journal of neurochemistry · 2025Article
- Exploring sphingolipid metabolism-related biomarkers for Parkinson's disease: a transcriptomic analysis.Frontiers in neurology · 2025Article
- Neutral sphingomyelinase 2: A promising drug target for CNS disease.Advances in pharmacology (San Diego, Calif.) · 2025Review
- Exploratory Analysis of the Association Between Plasma Ceramide Alterations and Cognitive Dysfunction in Parkinson's Disease.CNS neuroscience & therapeutics · 2024Article
- Nutritional roles and therapeutic potentials of dietary sphingomyelin in brain diseases.Journal of clinical biochemistry and nutrition · 2024Article
- Extracellular high molecular weight α-synuclein oligomers induce cell death by disrupting the plasma membrane.NPJ Parkinson's disease · 2023Article
- The Bidirectional Interplay of α-Synuclein with Lipids in the Central Nervous System and Its Implications for the Pathogenesis of Parkinson's Disease.International journal of molecular sciences · 2023Review
- Ceramide present in cholangiocarcinoma-derived extracellular vesicle induces a pro-inflammatory state in monocytes.Scientific reports · 2023Article
- Article
- Mysterious sphingolipids: metabolic interrelationships at the center of pathophysiology.Frontiers in physiology · 2023Review
- The regulatory mechanism and therapeutic potential of transcription factor EB in neurodegenerative diseases.CNS neuroscience & therapeutics · 2023Review
- Deregulation of mTORC1-TFEB axis in human iPSC model ofFrontiers in neuroscience · 2023Article
- Genetic modifiers of synucleinopathies-lessons from experimental models.Oxford open neuroscience · 2023Review
- 'Fly-ing' from rare to common neurodegenerative disease mechanisms.Trends in genetics : TIG · 2022Review
- Ceramide and Sphingosine-1-Phosphate in Neurodegenerative Disorders and Their Potential Involvement in Therapy.International journal of molecular sciences · 2022Review
- The Multiple Roles of Sphingomyelin in Parkinson's Disease.Biomolecules · 2021Review
- Article
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Authors and funding
15 authors at 5 institutions in 1 country.
Funding
Abstract
Parkinson's disease (PD) is a proteinopathy associated with the aggregation of α-synuclein and the formation of lipid-protein cellular inclusions, named Lewy bodies (LBs). LB formation results in impaired neurotransmitter release and uptake, which involve membrane traffic and require lipid synthesis and metabolism. Lipids, particularly ceramides, are accumulated in postmortem PD brains and altered in the plasma of PD patients. Autophagy is impaired in PD, reducing the ability of neurons to clear protein aggregates, thus worsening stress conditions and inducing neuronal death. The inhibition of ceramide synthesis by myriocin (Myr) in SH-SY5Y neuronal cells treated with preformed α-synuclein fibrils reduced intracellular aggregates, favoring their sequestration into lysosomes. This was associated with TFEB activation, increased expression of TFEB and LAMP2, and the cytosolic accumulation of LC3II, indicating that Myr promotes autophagy. Myr significantly reduces the fibril-related production of inflammatory mediators and lipid peroxidation and activates NRF2, which is downregulated in PD. Finally, Myr enhances the expression of genes that control neurotransmitter transport (SNARE complex, VMAT2, and DAT), whose progressive deficiency occurs in PD neurodegeneration. The present study suggests that counteracting the accumulation of inflammatory lipids could represent a possible therapeutic strategy for PD.
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