ReviewCNS neuroscience & therapeutics2018
Disrupted striatal neuron inputs and outputs in Huntington's disease.
Review in CNS neuroscience & therapeutics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
58 citing papers in PubMed, 96 citations in OpenAlex.
- The role of the globus pallidus subregions in the schizophrenia spectrum continuum.Molecular psychiatry · 2026Article
- From optical control to translational readiness: an evidence-tiered framework for optogenetics in neuromuscular and neurological disorders.Materials today. Bio · 2026Review
- Pridopidine Mediated Sigma-1 Receptor Activation and Therapeutic Implications in Neurodegenerative Diseases.Neurology international · 2026Review
- Inter-individual variation of cellular and gene-expression properties of the human striatum.bioRxiv : the preprint server for biology · 2026Article
- Silmitasertib, an FDA-designated orphan CK2 inhibitor, ameliorates neuropathology and motor dysfunction in a Huntington's disease mouse model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- From Balance to Breakdown: striatal PV interneurons in Huntington's disease and Autism Spectrum Disorder.Frontiers in cellular neuroscience · 2026Review
- Silmitasertib, an FDA-designated orphan CK2 Inhibitor, ameliorates neuropathology and motor dysfunction in a Huntington's disease mouse model.bioRxiv : the preprint server for biology · 2025Article
- The orexin/hypocretin system in dementia-related neurological disorders: a double-edged sword in cognitive impairment.Psychopharmacology · 2025Review
- Molecular Imbalances Between Striosome and Matrix Compartments Characterize the Pathogenesis and Pathophysiology of Huntington's Disease Model Mouse.International journal of molecular sciences · 2025Article
- The regulation of rhythmic locomotion by motor cortical and dopaminergic inputs in the mouse striatum.Molecular brain · 2025Article
- Therapeutic approaches targeting aging and cellular senescence in Huntington's disease.CNS neuroscience & therapeutics · 2024Review
- Construction of human 3D striato-nigral assembloids to recapitulate medium spiny neuronal projection defects in Huntington's disease.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- TRIM37 is a primate-specific E3 ligase for Huntingtin and accounts for the striatal degeneration in Huntington's disease.Science advances · 2024Article
- Postmortem neuropathology in early Huntington disease.Journal of neuropathology and experimental neurology · 2024Article
- Towards Standardizing Nomenclature in Huntington's Disease Research.Journal of Huntington's disease · 2024Review
- Local Administrations of Iron Oxide Nanoparticles in the Prefrontal Cortex and Caudate Putamen of Rats Do Not Compromise Working Memory and Motor Activity.Neurotoxicity research · 2023Article
- hESC-derived striatal progenitors grafted into a Huntington's disease rat model support long-term functional motor recovery by differentiating, self-organizing and connecting into the lesioned striatum.Stem cell research & therapy · 2023Article
- Cholinergic deficits selectively boost cortical intratelencephalic control of striatum in male Huntington's disease model mice.Nature communications · 2023Article
- Altered exocytosis of inhibitory synaptic vesicles at single presynaptic terminals of cultured striatal neurons in a knock-in mouse model of Huntington's disease.Frontiers in molecular neuroscience · 2023Article
- Pain in Huntington's disease and its potential mechanisms.Frontiers in aging neuroscience · 2023Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Huntington's disease (HD) is a hereditary progressive neurodegenerative disorder caused by a CAG repeat expansion in the gene coding for the protein huntingtin, resulting in a pathogenic expansion of the polyglutamine tract in the N-terminus of this protein. The HD pathology resulting from the mutation is most prominent in the striatal part of the basal ganglia, and progressive differential dysfunction and loss of striatal projection neurons and interneurons account for the progression of motor deficits seen in this disease. The present review summarizes current understanding regarding the progression in striatal neuron dysfunction and loss, based on studies both in human HD victims and in genetic mouse models of HD. We review evidence on early loss of inputs to striatum from cortex and thalamus, which may be the basis of the mild premanifest bradykinesia in HD, as well as on the subsequent loss of indirect pathway striatal projection neurons and their outputs to the external pallidal segment, which appears to be the basis of the chorea seen in early symptomatic HD. Later loss of direct pathway striatal projection neurons and their output to the internal pallidal segment account for the severe akinesia seen late in HD. Loss of parvalbuminergic striatal interneurons may contribute to the late dystonia and rigidity.
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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.