ArticlePloS one2011
Defects in very long chain fatty acid synthesis enhance alpha-synuclein toxicity in a yeast model of Parkinson's disease.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 49 citations in OpenAlex.
- From lipid function to dysfunction: Very long-chain fatty acids as emerging regulators of neuroinflammatory pathways.iScience · 2026Review
- Associations Between Diabetes Mellitus and Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- A crazy trio in Parkinson's disease: metabolism alteration, α-synuclein aggregation, and oxidative stress.Molecular and cellular biochemistry · 2025Review
- Exploratory Analysis of the Association Between Plasma Ceramide Alterations and Cognitive Dysfunction in Parkinson's Disease.CNS neuroscience & therapeutics · 2024Article
- The Contribution of Type 2 Diabetes to Parkinson's Disease Aetiology.International journal of molecular sciences · 2024Review
- Sporadic SNCA mutations A18T and A29S exhibit variable effects on protein aggregation, cell viability and oxidative stress.Molecular biology reports · 2023Article
- Review
- Genetic modifiers of synucleinopathies-lessons from experimental models.Oxford open neuroscience · 2023Review
- Article
- α-synuclein inhibits Snx3-retromer retrograde trafficking of the conserved membrane-bound proprotein convertase Kex2 in the secretory pathway of Saccharomyces cerevisiae.Human molecular genetics · 2022Article
- Neuropathology of SCA34 showing widespread oligodendroglial pathology with vacuolar white matter degeneration: a case study.Acta neuropathologica communications · 2021Article
- Review
- Genome-wide screen identifies curli amyloid fibril as a bacterial component promoting host neurodegeneration.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- A Gene Expression Signature to Predict Nucleotide Excision Repair Defects and Novel Therapeutic Approaches.International journal of molecular sciences · 2021Article
- Integrated Metabolomics and Proteomics Analysis Reveals Plasma Lipid Metabolic Disturbance in Patients With Parkinson's Disease.Frontiers in molecular neuroscience · 2020Article
- Panoramic Visualization of Circulating MicroRNAs Across Neurodegenerative Diseases in Humans.Molecular neurobiology · 2019Article
- Article
- Alpha-Synuclein Physiology and Pathology: A Perspective on Cellular Structures and Organelles.Frontiers in neuroscience · 2019Review
- Mitochondrial lipids in neurodegeneration.Cell and tissue research · 2017Review
- Ethanolamine and Phosphatidylethanolamine: Partners in Health and Disease.Oxidative medicine and cellular longevity · 2017Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
We identified three S. cerevisiae lipid elongase null mutants (elo1Δ, elo2Δ, and elo3Δ) that enhance the toxicity of alpha-synuclein (α-syn). These elongases function in the endoplasmic reticulum (ER) to catalyze the elongation of medium chain fatty acids to very long chain fatty acids, which is a component of sphingolipids. Without α-syn expression, the various elo mutants showed no growth defects, no reactive oxygen species (ROS) accumulation, and a modest decrease in survival of aged cells compared to wild-type cells. With (WT, A53T or E46K) α-syn expression, the various elo mutants exhibited severe growth defects (although A30P had a negligible effect on growth), ROS accumulation, aberrant protein trafficking, and a dramatic decrease in survival of aged cells compared to wild-type cells. Inhibitors of ceramide synthesis, myriocin and FB1, were extremely toxic to wild-type yeast cells expressing (WT, A53T, or E46K) α-syn but much less toxic to cells expressing A30P. The elongase mutants and ceramide synthesis inhibitors enhance the toxicity of WT α-syn, A53T and E46K, which transit through the ER, but have a negligible effect on A30P, which does not transit through the ER. Disruption of ceramide-sphingolipid homeostasis in the ER dramatically enhances the toxicity of α-syn (WT, A53T, and E46K).
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Registered trials
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