ArticleScience advances2023
Cognitive effects of thalamostriatal degeneration are ameliorated by normalizing striatal cholinergic activity.
Article in Science advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Early-Stage Corticostriatal Hyperactivity Impairs Cognitive Flexibility Alongside Striatal Cholinergic Dysfunction in an Alzheimer's Disease Model.Nature communications · 2026Article
- The parafascicular thalamus steers attention to facilitate learning.bioRxiv : the preprint server for biology · 2026Article
- Potential common pathogenesis of several neurodegenerative diseases.Neural regeneration research · 2026Article
- Early-Stage Corticostriatal Circuit Hyperactivity Impairs Cholinergic Function and Cognitive Flexibility in an Alzheimer's Model.bioRxiv : the preprint server for biology · 2026Article
- Dorsomedial striatal neuroinflammation causes excessive goal-directed action control by disrupting astrocyte function.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Distinct roles of two thalamostriatal systems in visually triggered decision-making in common marmosets.iScience · 2025Article
- Inflammaging and Immunosenescence in the Post-COVID Era: Small Molecules, Big Challenges.ChemMedChem · 2025Review
- Dynamic responses of striatal cholinergic interneurons control behavioral flexibility.Science advances · 2024Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The loss of neurons in parafascicular thalamus (Pf) and their inputs to dorsomedial striatum (DMS) in Lewy body disease (LBD) and Parkinson's disease dementia (PDD) have been linked to the effects of neuroinflammation. We found that, in rats, these inputs were necessary for both the function of striatal cholinergic interneurons (CINs) and the flexible encoding of the action-outcome (AO) associations necessary for goal-directed action, producing a burst-pause pattern of CIN firing but only during the remapping elicited by a shift in AO contingency. Neuroinflammation in the Pf abolished these changes in CIN activity and goal-directed control after the shift in contingency. However, both effects were rescued by either the peripheral or the intra-DMS administration of selegiline, a monoamine oxidase B inhibitor that we found also enhances adenosine triphosphatase activity in CINs. These findings suggest a potential treatment for the cognitive deficits associated with neuroinflammation affecting the function of the Pf and related structures.
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Registered trials
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.