ArticleMovement disorders : official journal of the Movement Disorder Society2023
Nicotine-Mediated Rescue of α-Synuclein Toxicity Requires Synaptic Vesicle Glycoprotein 2 in Drosophila.
Article in Movement disorders : official journal of the Movement Disorder Society, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 33 citations in OpenAlex.
- Structural Determinants of Synaptic Vesicle Protein 2C Ligand Selectivity and Their Impact on Dopamine Release.bioRxiv : the preprint server for biology · 2026Article
- SV2B is a crucial factor for early larval development in the silkworm, Bombyx mori.Insect science · 2026Article
- New insights into synaptic vesicle dysfunction in Parkinson's disease.Journal of Parkinson's disease · 2026Review
- Glycerol 3-phosphate acyltransferase exacerbates α-synuclein-induced toxicity by increasing lipid peroxidation.Nature communications · 2026Article
- Proposed mechanisms of neuroprotection for nicotine in Parkinson's disease.Journal of Parkinson's disease · 2025Review
- Role of extracellular vesicle-mediated neurodegeneration in substance use disorders.Current opinion in physiology · 2025Article
- Article
- A Review of the Protective Effects of Alkaloids against Alpha-synuclein Toxicity in Parkinson's Disease.Mini reviews in medicinal chemistry · 2025Review
- α-Synuclein species in plasma neuron-derived extracellular vesicles as biomarkers for iRBD.Annals of clinical and translational neurology · 2024Article
- Epidemiology of Parkinson's Disease: An Update.Current neurology and neuroscience reports · 2024Review
- Disruption of Dopamine Homeostasis Associated with Alteration of Proteins in Synaptic Vesicles: A Putative Central Mechanism of Parkinson's Disease Pathogenesis.Aging and disease · 2024Review
- Synaptic vesicle glycoprotein 2C enhances vesicular storage of dopamine and counters dopaminergic toxicity.The European journal of neuroscience · 2024Article
- Nicotinic Acetylcholine Receptors in Glial Cells as Molecular Target for Parkinson's Disease.Cells · 2024Review
- The potential of natural products to inhibit abnormal aggregation of α-Synuclein in the treatment of Parkinson's disease.Frontiers in pharmacology · 2024Review
- Synaptic Vesicle Glycoprotein 2C: a role in Parkinson's disease.Frontiers in cellular neuroscience · 2024Review
- Integrative analysis reveals a conserved role for the amyloid precursor protein in proteostasis during aging.Nature communications · 2023Article
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3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundParkinson's disease (PD) is characterized by α-synuclein aggregation and loss of dopamine neurons. Risk of PD arises due to a combination of genetic and environmental factors, which may interact, termed gene-environment (G×E) interactions. An inverse association between smoking and the risk of PD is well established, and a previous genome-wide G×E interaction study identified genetic variation in the synaptic-vesicle glycoprotein 2C (SV2C) locus as an important mediator of the degree to which smoking is inversely associated with PD.
objectiveWe sought to determine the mechanism of the smoking-SV2C interaction in a Drosophila model of PD.
methodsFlies expressing human α-synuclein in all neurons develop the hallmarks of PD, including motor dysfunction, loss of dopaminergic (DA) neurons, and formation of α-synuclein inclusions. We assessed the effects of increasing doses of nicotine on these parameters of neurodegeneration, in the presence or absence of knockdown of two Drosophila orthologues of SV2, hereafter referred to as SV2L1 and SV2L2.
resultsThe α-synuclein-expressing flies treated with nicotine had improved locomotion, DA neuron counts, and α-synuclein aggregation. However, in α-synuclein-expressing flies in which SV2L1 and SV2L2 were knocked down, nicotine failed to rescue neurodegeneration.
conclusionsThis work confirms a G×E interaction between nicotine and SV2, defines a role for this interaction in α-synuclein proteostasis, and suggests that future clinical trials on nicotine should consider genetic variation in SV2C. Furthermore, this provides proof of concept that our model can be used for the mechanistic study of G×E, paving the way for the investigation of additional G×E interactions or the identification of novel G×E. © 2022 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.
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