ArticleJournal of molecular neuroscience : MN2014
Sequence variants in SLC6A3, DRD2, and BDNF genes and time to levodopa-induced dyskinesias in Parkinson's disease.
Article in Journal of molecular neuroscience : MN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 70 citations in OpenAlex.
- Polymorphisms of the dopamine metabolic and signaling pathways are associated with susceptibility to motor levodopa-induced complications (MLIC) in Parkinson's disease: a systematic review and meta-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022Pooled it
- A systematic review and integrative approach to decode the common molecular link between levodopa response and Parkinson's disease.BMC medical genomics · 2017Pooled it
- Presence of recombination hotspots throughout SLC6A3.PloS one · 2019Trial
- Dopamine Pathway and Parkinson's Risk Variants Are Associated with Levodopa-Induced Dyskinesia.Movement disorders : official journal of the Movement Disorder Society · 2024Article
- A Molecular Framework for Delirium.The Neurohospitalist · 2024Review
- Role of dopamine agonists in Parkinson's disease therapy.Journal of neural transmission (Vienna, Austria : 1996) · 2023Review
- Pharmacogenomics-a New Frontier for Individualized Treatment of Parkinson's Disease.Current neuropharmacology · 2023Review
- BDNF rs6265 Genotype Influences Outcomes of Pharmacotherapy and Subthalamic Nucleus Deep Brain Stimulation in Early-Stage Parkinson's Disease.Neuromodulation : journal of the International Neuromodulation Society · 2022Article
- The Role of Single Nucleotide Polymorphisms of Monoamine Oxidase B, Dopamine D2 Receptor, and DOPA Decarboxylase Receptors Among Patients Treated for Parkinson's Disease.Journal of molecular neuroscience : MN · 2022Article
- The dopamine transporter gene SLC6A3: multidisease risks.Molecular psychiatry · 2022Article
- FunctionalParkinson's disease · 2022Article
- A Roadmap for Future Parkinson's Pharmacogenomics in Asia.Frontiers in aging neuroscience · 2022Article
- Polymorphisms of Dopamine Receptor Genes and Parkinson's Disease: Clinical Relevance and Future Perspectives.International journal of molecular sciences · 2021Review
- Circuit Mechanisms of L-DOPA-Induced Dyskinesia (LID).Frontiers in neuroscience · 2021Review
- Pharmacogenetic profile and the development of the dyskinesia induced by levodopa-therapy in Parkinson's disease patients: a population-based cohort study.Molecular biology reports · 2020Article
- Gene polymorphisms and motor levodopa-induced complications in Parkinson's disease.Brain and behavior · 2020Article
- MTOR Pathway-Based Discovery of Genetic Susceptibility to L-DOPA-Induced Dyskinesia in Parkinson's Disease Patients.Molecular neurobiology · 2019Article
- Dopaminergic Pathway Genes Influence Adverse Events Related to Dopaminergic Treatment in Parkinson's Disease.Frontiers in pharmacology · 2019Article
- Allelic variant inPeerJ · 2019Article
- Dyskinesias and levodopa therapy: why wait?Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Levodopa-induced dyskinesias (LID) present a common but elusive complication of levodopa therapy in Parkinson's disease (PD). In order to identify genetic factors associated with LID, 352 (213 males) levodopa-treated Israeli PD patients were genotyped for 34 polymorphisms within three candidate genes affecting dopaminergic activity and synaptic plasticity: dopamine transporter gene (DAT1 or SLC6A3) [14 single nucleotide polymorphisms (SNPs) and 40-bp variable number tandem repeat (VNTR)], DRD2 [11 SNPs and dinucleotide CA short tandem repeat (STR)], and BDNF (7 SNPs). A comparison of patients with and without LID was performed by applying a time-oriented approach, with survival analyses evaluating LID development hazard rate over time [Cox proportional hazards and accelerated failure time (AFT) lognormal models]. Overall, 192 (54.5 %) participants developed LID, with a mean latency of 5.0 (±4.5) years. After adjusting for gender, age at PD onset, duration of symptoms prior to levodopa exposure, and multiple testing correction, one SNP in SLC6A3 (with 81 % genotyping success) was significantly associated with LID latency: the C allele of the rs393795 extended the time to LID onset, time ratio = 4.96 (95 % CI, 2.3-10.9; p = 4.1 × 10(-5)). This finding should be validated in larger, ethnically diverse PD populations, and the biological mechanism should be explored.
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Registered trials
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