Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (840 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Syndromes which feature dyskinesias as a cardinal manifestation of the disease process. Included in this category are degenerative, hereditary, post-infectious, medication-induced, post-inflammatory, and post-traumatic conditions.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Movement Disorder; Dyskinesia Syndromes; Dyskinesia Syndrome; Movement Disorder Syndromes; Movement Disorder Syndrome; Etat Marbre; Status Marmoratus.
Where it fits in the MeSH classification
- Broader topics
- Central Nervous System Diseases
- Narrower topics
- Akathisia, Drug-Induced; Angelman Syndrome; Dyskinesias; Dystonic Disorders; Essential Tremor; Hepatolenticular Degeneration; Multiple System Atrophy; Pantothenate Kinase-Associated Neurodegeneration; Parkinsonian Disorders; Supranuclear Palsy, Progressive; Tic Disorders
- See also
- Psychomotor Disorders; Dyskinesias
Related concepts
- Dyskinesias
Research landscape
PubMed indexes 180,684 records tagged with the MeSH heading “Movement Disorders” (counts retrieved 2026-10-29). 44,380 of them (24.6%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 54,967 records.
Reviews account for 31,694 records (17.5%) and meta-analyses for 2,227. Randomized controlled trials number 4,288 (2.4%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 45,596 |
| 2000-2009 | 35,741 |
| 2010-2019 | 54,967 |
| 2020 onward | 44,380 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 31,694 | 17.5% |
| Meta-analyses | 2,227 | 1.2% |
| Randomized controlled trials | 4,288 | 2.4% |
Method: PubMed query "Movement Disorders"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in neuroscience
Neuroscience draws on tools with different strengths: cellular and animal work can manipulate circuits directly, while human imaging and electrophysiology observe the living brain at lower resolution. Small imaging studies are prone to false positives, and findings in animals do not always carry over to people. Clinical neurology and psychiatry rely on trials and cohort studies whose outcomes are often symptom scales. Check the species, the sample size, how the outcome was measured and whether results were replicated.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Leucine-rich repeat kinase 2 impairs the release sites of Parkinson's disease vulnerable dopamine axons | 2026 | Research article Design not recorded in structured metadata | 5 | cc by PMID 42660892 · DOI · PMC13522591 |
| Parkinson's disease-associated PINK1 loss disrupts ensheathing glia and causes dopaminergic neuron synapse loss | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42592915 · DOI · PMC13472629 |
| Cholesterol nose-to-brain delivery as a possible therapeutic strategy in Huntington's disease | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42552550 · DOI · PMC13435458 |
| Nitric oxide signaling and mitophagy in Parkinson's disease: implications for aerobic exercise-related neuroprotection | 2027 | Review article Design not recorded in structured metadata | 0 | cc by PMID 42734454 · DOI · PMC13667388 |
Leucine-rich repeat kinase 2 impairs the release sites of Parkinson's disease vulnerable dopamine axons [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Parkinson's disease (PD) is defined pathologically by loss of dopamine-producing neurons in the substantia nigra pars compacta (SNc).
- Closing excerpt
- Together, these findings highlight a subtype-specific, cell-autonomous mechanism by which pathogenic LRRK2 impairs PD-vulnerable nigrostriatal synapses and provide a framework for therapeutic strategies targeting early synaptic deficits in PD.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (156 words)
Parkinson's disease (PD) is defined pathologically by loss of dopamine-producing neurons in the substantia nigra pars compacta (SNc). Yet synaptic dysfunction emerges much earlier, making it essential to define the mechanisms that drive early nigrostriatal deregulation. In the SNc, molecularly distinct dopamine neuron subtypes show differential susceptibility to PD. Here, we used intersectional genetic mouse models to determine how the PD-linked kinase LRRK2 affects vulnerable dopamine subtypes. Immunofluorescence and proximity-labeling proteomics revealed enriched LRRK2 expression in vulnerable dopamine neuron subclusters. High-resolution imaging showed that pathogenic LRRK2 disrupts presynaptic release-site organization in vulnerable dopamine axons, leading to reduced spontaneous and evoked striatal dopamine release in vivo. Proteomic analyses further showed that mutant LRRK2 increases phosphorylation of RAB3 proteins, impairing their interaction with the active-zone effectors RIM1 and RIM2. Together, these findings highlight a subtype-specific, cell-autonomous mechanism by which pathogenic LRRK2 impairs PD-vulnerable nigrostriatal synapses and provide a framework for therapeutic strategies targeting early synaptic deficits in PD.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42660892 · DOI · PMC13522591
Parkinson's disease-associated PINK1 loss disrupts ensheathing glia and causes dopaminergic neuron synapse loss [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Parkinson's disease (PD) is commonly associated with the loss of dopaminergic neurons in the substantia nigra, but many other cell types are affected even before neuron loss occurs.
- Closing excerpt
- Our work highlights the essential role of glial support cells in the pathogenesis of PD and identifies vesicle trafficking within these cells in disease progression.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (219 words)
Parkinson's disease (PD) is commonly associated with the loss of dopaminergic neurons in the substantia nigra, but many other cell types are affected even before neuron loss occurs. Recent studies have linked oligodendrocytes to early stages of PD, though their precise role is still unclear. PINK1 is mutated in familial PD, and through unbiased single-cell sequencing of the entire brain of Drosophila Pink1 models, we observed significant gene deregulation in ensheathing glia (EG), cells that share functional similarities with oligodendrocytes. We found that the loss of Pink1 leads to abnormalities in EG, similar to the reactive response of EG seen upon nerve injury. Using cell-type-specific transcriptomics, we identified deregulated genes in EG as potential functional modifiers. Specifically downregulating two trafficking factors in EG, Vps35 and Vps13, also mutated in PD, was sufficient to rescue neuronal function and protect against dopaminergic synapse loss. Our findings demonstrate that Pink1 loss in neurons triggers an injury-like response in EG, and that Pink1 loss in EG, in turn, disrupts neuronal function. Vesicle trafficking components, which may regulate membrane interactions between organelles in EG, seem to play a role in maintaining neuronal health and ultimately preventing dopaminergic synapse loss. Our work highlights the essential role of glial support cells in the pathogenesis of PD and identifies vesicle trafficking within these cells in disease progression.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42592915 · DOI · PMC13472629
Cholesterol nose-to-brain delivery as a possible therapeutic strategy in Huntington's disease [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundHuntington's disease (HD) is a genetically dominant neurodegenerative disorder characterized by several pathological mechanisms, including the disruption of brain cholesterol homeostasis.
- Closing excerpt
- ConclusionsThe findings support the effectiveness of cholesterol supplementation as a therapeutic strategy for HD and indicate the translational potential of nose-to-brain cholesterol delivery.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (246 words)
BackgroundHuntington's disease (HD) is a genetically dominant neurodegenerative disorder characterized by several pathological mechanisms, including the disruption of brain cholesterol homeostasis. In several HD animal models, brain cholesterol biosynthesis and levels are reduced. Since circulating cholesterol cannot reach the brain, providing exogenous cholesterol has been shown to improve HD phenotypes. However, the methods used for cholesterol delivery were invasive and not easily transferable to clinical practice.MethodsCholesterol-enriched liposomes were developed by using freeze-and-thaw methods and were administered to R6/2 mice through a single or repeated intranasal administrations. Deuterated-cholesterol was used to discriminate exogenous from endogenous cholesterol. Exogenous cholesterol accumulation and distribution, as well as the levels of cholesterol precursors and metabolites, were measured using mass spectrometry. Behavioral tests, real-time PCR analysis, and immunostaining of mutant HTT (muHTT) aggregates were performed to verify the therapeutic effects of liposomes. Plasma neurofilament levels were measured by Simoa-Quanterix assay.ResultsWe developed and characterized freeze-and-thaw liposomes. Then, we demonstrate that the exogenous cholesterol can spread throughout the entire brain following intranasal administration of cholesterol-enriched liposomes. Furthermore, repeated intranasal treatments with liposomes result in a full restoration of cognitive decline, and delayed the onset of coordination and motor impairment as well as the loss of muscular strength in the early stages of the disease. Cholesterol supplementation also reduced the plasma level of neurofilament light chain and promoted the clearance of muHTT aggregates.ConclusionsThe findings support the effectiveness of cholesterol supplementation as a therapeutic strategy for HD and indicate the translational potential of nose-to-brain cholesterol delivery.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42552550 · DOI · PMC13435458
Nitric oxide signaling and mitophagy in Parkinson's disease: implications for aerobic exercise-related neuroprotection [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Parkinson's disease is strongly associated with mitochondrial dysfunction and impaired mitochondrial quality control, including defective mitophagy.
- Closing excerpt
- Overall, aerobic exercise is a plausible modulator of mitophagy-related pathways in Parkinson's disease, and nitric oxide is a credible contributor to this effect; however, the current evidence supports a multi-node, context-dependent model rather than a simple linear mechanism.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (219 words)
Parkinson's disease is strongly associated with mitochondrial dysfunction and impaired mitochondrial quality control, including defective mitophagy. Aerobic exercise is increasingly recognized as a safe and accessible intervention that can improve motor and non-motor outcomes in Parkinson's disease and may also engage mechanisms relevant to disease modification. In this review, we propose a context-dependent framework in which aerobic exercise reshapes nitric oxide signaling toward a more adaptive profile, characterized by relatively moderate, transient, and spatially restricted nitric oxide bioactivity, and we discuss how this shift may influence mitochondrial biogenesis, mitophagy initiation, and autophagic flux regulation. Rather than treating nitric oxide as uniformly protective or deleterious, we argue that its biological effects in Parkinson's disease depend on source, concentration, duration, subcellular localization, cellular target, and surrounding redox milieu. However, direct evidence that exercise-derived nitric oxide activates these pathways in Parkinson's disease-relevant neural tissue is still limited. We further highlight major translational gaps, including cell-type and brain-region heterogeneity, incomplete definition of exercise dose-response relationships, and the lack of validated in vivo biomarkers of neuronal mitophagy and nitric oxide dynamics in patients with Parkinson's disease. Overall, aerobic exercise is a plausible modulator of mitophagy-related pathways in Parkinson's disease, and nitric oxide is a credible contributor to this effect; however, the current evidence supports a multi-node, context-dependent model rather than a simple linear mechanism.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42734454 · DOI · PMC13667388
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Temporal trends in the prevalence of Parkinson's disease from 1980 to 2023: a systematic review and meta-analysis [5]
- Research article Physical exercise for people with Parkinson's disease: a systematic review and network meta-analysis [6]
- Research article Risk of Dementia in Parkinson's Disease: A Systematic Review and Meta-Analysis [7]
- Research article Analysis of biomarkers in speculative CNS-enriched extracellular vesicles for parkinsonian disorders: a comprehensive systematic review and diagnostic meta-analysis [8]
- Research article Machine learning-based meta-analysis reveals gut microbiome alterations associated with Parkinson's disease [9]
- Research article Effects of transcranial direct current stimulation alone and in combination with rehabilitation therapies on gait and balance among individuals with Parkinson's disease: a systematic review and meta-analysis [10]
References
- Chen C, He Q, Tombesi G, Napier E, Jaconelli M, Moreno-Ramos OA, et al.. Leucine-rich repeat kinase 2 impairs the release sites of Parkinson's disease vulnerable dopamine axons. . 2026. PMID 42660892 · DOI · PMC13522591
- Ghezzi L, Kuenen S, Pech U, Schoovaerts N, Kilic A, Poovathingal S, et al.. Parkinson's disease-associated PINK1 loss disrupts ensheathing glia and causes dopaminergic neuron synapse loss. . 2026. PMID 42592915 · DOI · PMC13472629
- Favagrossa M, Passoni A, Valenza M, Di Prisco D, Birolini G, Villa M, et al.. Cholesterol nose-to-brain delivery as a possible therapeutic strategy in Huntington's disease. . 2026. PMID 42552550 · DOI · PMC13435458
- Zhou Y, Wu Y. Nitric oxide signaling and mitophagy in Parkinson's disease: implications for aerobic exercise-related neuroprotection. . 2027. PMID 42734454 · DOI · PMC13667388
- Zhu J, Cui Y, Zhang J, Yan R, Su D, Zhao D, et al.. Temporal trends in the prevalence of Parkinson's disease from 1980 to 2023: a systematic review and meta-analysis. Lancet Healthy Longev. 2024. PMID 38945129 · DOI
- Ernst M, Folkerts AK, Gollan R, Lieker E, Caro-Valenzuela J, Adams A, et al.. Physical exercise for people with Parkinson's disease: a systematic review and network meta-analysis. Cochrane Database Syst Rev. 2024. PMID 38588457 · DOI · PMC11001292
- Gibson LL, Weintraub D, Lemmen R, Perera G, Chaudhuri KR, Svenningsson P, et al.. Risk of Dementia in Parkinson's Disease: A Systematic Review and Meta-Analysis. Mov Disord. 2024. PMID 39036849 · DOI
- Taha HB, Bogoniewski A. Analysis of biomarkers in speculative CNS-enriched extracellular vesicles for parkinsonian disorders: a comprehensive systematic review and diagnostic meta-analysis. J Neurol. 2024. PMID 38103086 · DOI · PMC10973014
- Romano S, Wirbel J, Ansorge R, Schudoma C, Ducarmon QR, Narbad A, et al.. Machine learning-based meta-analysis reveals gut microbiome alterations associated with Parkinson's disease. Nat Commun. 2025. PMID 40335465 · DOI · PMC12059030
- Nguyen TXD, Mai PT, Chang YJ, Hsieh TH. Effects of transcranial direct current stimulation alone and in combination with rehabilitation therapies on gait and balance among individuals with Parkinson's disease: a systematic review and meta-analysis. J Neuroeng Rehabil. 2024. PMID 38373966 · DOI · PMC10875882
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.