ReviewFrontiers in immunology2023
Levodopa-induced dyskinesia: interplay between the N-methyl-D-aspartic acid receptor and neuroinflammation.
Review in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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
12 citing papers in PubMed, 14 citations in OpenAlex.
- Parkinson's disease: pathogenesis and therapeutic strategies.Molecular biomedicine · 2026Review
- Levodopa exposure and nigral neuroinflammation in parkinsonian disorders: A postmortem study of 63 cases.Scientific reports · 2025Article
- Crinis Carbonisatus-Derived Carbon Dot Suspension Alleviates Temporal Lobe Epilepsy.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Involvement of Neuroinflammation and Oxidative Stress in L-DOPA-Induced Dyskinesia in Parkinson's Disease: Role of Renin-Angiotensin System and ROCK Pathway.Antioxidants (Basel, Switzerland) · 2025Review
- Stigmasterol Alleviates Levodopa-Induced Dyskinesia in 6-OHDA-Induced Parkinsonian Rats.Neurochemical research · 2025Article
- Regulating astrocytic activity in the dorsal striatum mitigates L-dopa-induced dyskinesia in Parkinson's disease.Scientific reports · 2025Article
- The Role of ΔFosB in the Pathogenesis of Levodopa-Induced Dyskinesia: Mechanisms and Therapeutic Strategies.Molecular neurobiology · 2025Review
- Metabolomics in Parkinson's Disease and Correlation with Disease State.Metabolites · 2025Review
- NMDA receptors in neurodegenerative diseases: mechanisms and emerging therapeutic strategies.Frontiers in aging neuroscience · 2025Review
- Levodopa-induced dyskinesia: brain iron deposition as a new hypothesis.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024Review
- Review
- Neuroinflammation and Dyskinesia: A Possible Causative Relationship?Brain sciences · 2024Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is a common neurodegenerative disorder of middle-aged and elderly people, clinically characterized by resting tremor, myotonia, reduced movement, and impaired postural balance. Clinically, patients with PD are often administered levodopa (L-DOPA) to improve their symptoms. However, after years of L-DOPA treatment, most patients experience complications of varying severity, including the "on-off phenomenon", decreased efficacy, and levodopa-induced dyskinesia (LID). The development of LID can seriously affect the quality of life of patients, but its pathogenesis is unclear and effective treatments are lacking. Glutamic acid (Glu)-mediated changes in synaptic plasticity play a major role in LID. The N-methyl-D-aspartic acid receptor (NMDAR), an ionotropic glutamate receptor, is closely associated with synaptic plasticity, and neuroinflammation can modulate NMDAR activation or expression; in addition, neuroinflammation may be involved in the development of LID. However, it is not clear whether NMDA receptors are co-regulated with neuroinflammation during LID formation. Here we review how neuroinflammation mediates the development of LID through the regulation of NMDA receptors, and assess whether common anti-inflammatory drugs and NMDA receptor antagonists may be able to mitigate the development of LID through the regulation of central neuroinflammation, thereby providing a new theoretical basis for finding new therapeutic targets for LID.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.