ArticleBiological psychiatry2025
Interneuron Loss and Microglia Activation by Transcriptome Analyses in the Basal Ganglia of Tourette Disorder.
Article in Biological psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Tourette syndrome.Nature reviews. Disease primers · 2026Review
- Jingxin Zhidong Formula Alleviates Tic Disorder via Modulation of Microglial IKK/NF-κB Signaling and Striatal Neurotransmitter Homeostasis.Brain and behavior · 2026Article
- Tourette disorder features pervasive neuronal and glial transcriptional remodeling in the dorsolateral prefrontal cortex.bioRxiv : the preprint server for biology · 2026Article
- [Volatile oil fromNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- DNA variants affecting chromatin structure are key to the genetic architecture of obsessive compulsive disorder.Epigenetics & chromatin · 2026Article
- The potential role of aberrant microglial synaptic pruning in the neurodevelopmental pathogenesis of tourette syndrome.Frontiers in neuroscience · 2026Review
- Tics severity in Tourette syndrome associated with higher glutamatergic activity in the anterior cingulate cortex.Brain communications · 2026Article
- A Celsr3 Mutation Linked to Tourette Disorder Disrupts Cortical Dendritic Patterning and Striatal Cholinergic Interneuron Excitability.International journal of molecular sciences · 2025Article
- Yinhua Gouteng decoction alleviates tic disorder symptoms by modulating neuro-inflammation in a rat model.Frontiers in immunology · 2025Article
- Peripheral blood transcriptomics identifies cohesin-chromatin and immune dysregulation in tics and Tourette syndrome.Frontiers in neurologyArticle
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Abstract
backgroundTourette disorder (TS) is characterized by motor hyperactivity and tics that are believed to originate in the basal ganglia. Postmortem immunocytochemical analyses has revealed decreases in cholinergic (CH), as well as parvalbumin and somatostatin GABA (gamma-aminobutyric acid) interneurons (INs) within the caudate/putamen of individuals with TS.
methodsWe obtained transcriptome and open chromatin datasets by single-nucleus RNA sequencing and single-nucleus ATAC sequencing, respectively, from caudate/putamen postmortem specimens of 6 adults with TS and 6 matched normal control subjects. Differential gene expression and differential chromatin accessibility analyses were performed in identified cell types.
resultsThe data reproduced the known cellular composition of the human striatum, including a majority of medium spiny neurons (MSNs) and small populations of GABA-INs and CH-INs. INs were decreased by ∼50% in TS brains, with no difference in other cell types. Differential gene expression analysis suggested that mitochondrial oxidative metabolism in MSNs and synaptic adhesion and function in INs were both decreased in subjects with TS, while there was activation of immune response in microglia. Gene expression changes correlated with changes in activity of cis-regulatory elements, suggesting a relationship of transcriptomic and regulatory abnormalities in MSNs, oligodendrocytes, and astrocytes of TS brains.
conclusionsThis initial analysis of the TS basal ganglia transcriptome at the single-cell level confirms the loss and synaptic dysfunction of basal ganglia INs, consistent with in vivo basal ganglia hyperactivity. In parallel, oxidative metabolism was decreased in MSNs and correlated with activation of microglia cells, which is attributable at least in part to dysregulated activity of putative enhancers, implicating altered epigenomic regulation in TS.
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