ArticleHuman brain mapping2015
Dopaminergic basis for impairments in functional connectivity across subdivisions of the striatum in Parkinson's disease.
Article in Human brain mapping, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.
- Quantitative Susceptibility Mapping and Resting State Network Analyses in Parkinsonian Phenotypes-A Systematic Review of the Literature.Frontiers in neural circuits · 2019Pooled it
- Temporal Interference Stimulation Modulates Resting State Functional Connectivity of Motor Circuit in Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2026Trial
- Individualized cortico-basal ganglia-thalamo-cortical circuit dysfunction links striatal dopaminergic loss to motor symptom severity in Parkinson's disease.NPJ Parkinson's disease · 2026Article
- Behavior- and Cell Type-Specific Cortico-Striatal Decoupling in a Parkinson's Disease-Like Mouse Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Dopaminergic modulation and dosage effects on brain state dynamics and working memory component processes in Parkinson's disease.Nature communications · 2025Article
- Alterations in neuroplasticity and functional connectivity of striatal subregions in Bell's palsy patients after acupuncture.Frontiers in neurology · 2025Article
- Dopamine alters functional gradients in Parkinson's disease.Imaging neuroscience (Cambridge, Mass.) · 2025Article
- Dynamic properties in functional connectivity changes and striatal dopamine deficiency in Parkinson's disease.Human brain mapping · 2024Article
- Chemically Synthesized AgNPs andJournal of fungi (Basel, Switzerland) · 2023Article
- Temporal and spatial variability of dynamic microstate brain network in early Parkinson's disease.NPJ Parkinson's disease · 2023Article
- Altered functional connectivity associated with striatal dopamine depletion in Parkinson's disease.Cerebral cortex communications · 2023Article
- Motor learning is independent of effects of subthalamic deep brain stimulation on motor execution.Brain communications · 2023Article
- Dopaminergic medication normalizes aberrant cognitive control circuit signalling in Parkinson's disease.Brain : a journal of neurology · 2022Article
- Functional connectivity of the cortico-subcortical sensorimotor loop is modulated by the severity of nigrostriatal dopaminergic denervation in Parkinson's Disease.NPJ Parkinson's disease · 2022Article
- Longitudinal clustering analysis and prediction of Parkinson's disease progression using radiomics and hybrid machine learning.Quantitative imaging in medicine and surgery · 2022Article
- Altered Intrinsic Regional Spontaneous Brain Activity in Patients With Severe Obesity and Meibomian Gland Dysfunction: A Resting-State Functional Magnetic Resonance Imaging Study.Frontiers in human neuroscience · 2022Article
- Narrow doorways alter brain connectivity and step patterns in isolated REM sleep behaviour disorder.NeuroImage. Clinical · 2022Article
- G-protein coupled receptor 88 knockdown in the associative striatum reduces psychiatric symptoms in a translational male rat model of Parkinson disease.Journal of psychiatry & neuroscience : JPN · 2021Article
- More Than Just Static: Dynamic Functional Connectivity Changes of the Thalamic Nuclei to Cortex in Parkinson's Disease With Freezing of Gait.Frontiers in neurology · 2021Article
- Motor Symptom Lateralization Influences Cortico-Striatal Functional Connectivity in Parkinson's Disease.Frontiers in neurology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathological hallmark of Parkinson's disease is the degeneration of dopaminergic nigrostriatal neurons, leading to depletion of striatal dopamine. Recent neuroanatomical work has identified pathways for communication across striatal subdivisions, suggesting that the striatum provides a platform for integration of information across parallel corticostriatal circuits. The aim of this study was to investigate whether dopaminergic dysfunction in Parkinson's disease was associated with impairments in functional connectivity across striatal subdivisions, which could potentially reflect reduced integration across corticostriatal circuits. Utilizing resting-state functional magnetic resonance imaging (fMRI), we analyzed functional connectivity in 39 patients with Parkinson's disease, both "on" and "off" their regular dopaminergic medications, along with 40 age-matched healthy controls. Our results demonstrate widespread impairments in connectivity across subdivisions of the striatum in patients with Parkinson's disease in the "off" state. The administration of dopaminergic medication significantly improved connectivity across striatal subdivisions in Parkinson's disease, implicating dopaminergic deficits in the pathogenesis of impaired striatal interconnectivity. In addition, impaired striatal interconnectivity in the Parkinson's disease "off" state was associated with pathological decoupling of the striatum from the thalamic and sensorimotor (SM) networks. Specifically, we found that although the strength of striatal interconnectivity was positively correlated with both (i) the strength of internal thalamic connectivity, and (ii) the strength of internal SM connectivity, in both healthy controls and the Parkinson's disease "on" state, these relationships were absent in Parkinson's disease when in the "off" state. Taken together our findings emphasize the central role of dopamine in integrated striatal function and the pathological consequences of striatal dopamine denervation in Parkinson's disease.
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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 OpenQuestion graph.