ArticleNPJ Parkinson's disease2025
Motor cortical neuronal hyperexcitability associated with α-synuclein aggregation.
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 9 papers.
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Who cites it
9 citing papers in PubMed.
- Motor Cortex Hyperexcitability Is Coupled to Neuromuscular Dysfunction in Aged Mice.Aging cell · 2026Article
- Immune-mediated excitotoxicity in brain disorders.Nature reviews. Immunology · 2026Review
- α-Synuclein pathology differentially alters T-type calcium currents in vulnerable and resilient substantia nigra dopaminergic subpopulations.bioRxiv : the preprint server for biology · 2026Article
- Cell-Type-Selective Cortical Pathology and Functional Deficits in Synucleinopathy.bioRxiv : the preprint server for biology · 2026Article
- Molecular Pathogenesis of Memory Impairment in Parkinson's Disease: An Exploration of Underlying Mechanisms.Health science reports · 2026Article
- Magnetoencephalography-based prediction of longitudinal symptom progression in Parkinson's disease.NPJ Parkinson's disease · 2026Article
- Microscale dysfunction and mesoscale compensation in degenerating neuronal networks.Network neuroscience (Cambridge, Mass.) · 2026Article
- The extent of alpha-synuclein aggregate accumulation in neurons varies depending on the type of neurotransmitter they release.Scientific reports · 2025Article
- Cortical α-synuclein pathology induces cell autonomous neuronal hypoactivity and compensatory circuit changes in a model of early Lewy body dementia.bioRxiv : the preprint server for biology · 2025Article
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Abstract
ΑBSTRACT: In Parkinson's disease (PD), Lewy pathology deposits in the cerebral cortex, but how the pathology disrupts cortical circuit integrity and function remains poorly understood. To begin to address this question, we injected α-synuclein (αSyn) preformed fibrils (PFFs) into the dorsolateral striatum of mice to seed αSyn pathology in the cortical cortex and induce degeneration of midbrain dopaminergic neurons. We reported that αSyn aggregates accumulate in the motor cortex in a layer- and cell-subtype-specific pattern. Specifically, αSyn aggregates-bearing intratelencephalic neurons (ITNs) showed hyperexcitability, increased input resistance, and decreased cell capacitance, which were associated with impaired HCN channel function. Morphologically, the αSyn aggregates-bearing ITNs showed shrinkage of cell bodies and loss of dendritic spines. Last, we showed that partial dopamine depletion is not sufficient to alter thalamocortical transmission to cortical pyramidal neurons. Our results provide a novel mechanistic understanding of cortical circuit dysfunction in PD.
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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.