ArticleCommunications biology2022
Discovery of levodopa-induced dyskinesia-associated genes using genomic studies in patients and Drosophila behavioral analyses.
Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Evolutionary trajectories of teleost olfactory signaling genes shaped by long-term redundancy after whole-genome duplication.iScience · 2026Article
- Behavioral screening defines the molecular Parkinsonism-related subgroups in Drosophila.Nature communications · 2026Article
- Capsaicin responses in Drosophila: Exploring the possibility of establishing a new Non-TRPV1 model.Biochemistry and biophysics reports · 2026Review
- Adenylyl cyclase 2 expression and function in neurological diseases.CNS neuroscience & therapeutics · 2024Review
- Neuroinflammation and Dyskinesia: A Possible Causative Relationship?Brain sciences · 2024Review
- Diabetic sensory neuropathy and insulin resistance are induced by loss of UCHL1 in Drosophila.Nature communications · 2024Article
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although levodopa is the most effective medication for Parkinson's disease, long-term levodopa treatment is largely compromised due to late motor complications, including levodopa-induced dyskinesia (LID). However, the genetic basis of LID pathogenesis has not been fully understood. Here, we discover genes pathogenic for LID using Drosophila genetics and behavioral analyses combined with genome-wide association studies on 578 patients clinically diagnosed with LID. Similar to the therapeutic effect of levodopa in patients, acute levodopa treatments restore the motor defect of Parkinson's disease model flies, while prolonged treatments cause LID-related symptoms, such as increased yawing, freezing and abrupt acceleration of locomotion. These symptoms require dopamine 1-like receptor 1 and are induced by neuronal overexpression of the receptor. Among genes selected from our analyses in the patient genome, neuronal knockdown of adenylyl cyclase 2 suppresses the levodopa-induced phenotypes and the receptor overexpression-induced symptoms in Drosophila. Together, our study provides genetic insights for LID pathogenesis through the D1-like receptor-adenylyl cyclase 2 signaling axis.
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