ArticleNPJ Parkinson's disease2025
Parkinsonism disrupts cortical function by dysregulating oscillatory, network and synaptic activity of parvalbumin positive interneurons.
Article in NPJ Parkinson's disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- Restless Legs Syndrome: A Network Model of Iron-Dependent Neuromodulation-A Narrative Review.Brain sciences · 2026Review
- Braking Parkinson's progression: the hypothetical druggable role of striatal parvalbumin interneurons.NPJ Parkinson's disease · 2026Review
- Chloride Homeostasis Failure in Human Disease: KCC2/NKCC1 Microdomain Dysfunction as a Driver of Cortical Network Collapse.International journal of molecular sciences · 2026Review
- Magnetoencephalography-based prediction of longitudinal symptom progression in Parkinson's disease.NPJ Parkinson's disease · 2026Article
- Remodeling of Perineuronal Nets in the Striato-Cortical Axis in L-DOPA-Induced Dyskinesia Rat Model.International journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Identifying novel and accessible therapeutic targets for Parkinson's Disease (PD) remains a pressing goal. Growing evidence implicates cortical dysfunctions in PD-related symptoms, yet the mechanisms-especially those involving parvalbumin-positive interneurons (PV-INs), key regulators of brain oscillations and plasticity-are not fully understood. In this study, we investigate how PD alters PV-IN network and cortical oscillatory dynamics using the 6-hydroxydopamine (6-OHDA) mouse model. Through an integrated approach combining electrophysiological recordings, wide-field calcium imaging, and histological analysis, we reveal a profound cascade of cortical changes. These include pathological hyperactivity above 100 Hz during movement and severe disruptions in PV-IN connectivity across the motor cortex. Synaptic imbalances and microglial activation further point to a multifaceted cortical response to dopaminergic degeneration, revealing inhibitory dysfunction, oscillatory instability, structural remodeling, and neuroinflammation. Our results link PD to cortical instability and highlight cortical plasticity as a promising target for therapeutic intervention.
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Registered trials
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