ArticleNature communications2023
Transcriptional vulnerabilities of striatal neurons in human and rodent models of Huntington's disease.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- Improving reproducibility of differentially expressed genes in single-cell transcriptomic studies of neurodegenerative diseases through meta-analysis.Nature communications · 2025Pooled it
- Spatial transcriptomics reveal developmental dynamics of the human cerebral cortex and striatum.Science China. Life sciences · 2026Article
- Cortistatin as a modulator of inflammatory and mitochondrial dysfunction in Huntington´s disease.Journal of neuroinflammation · 2026Article
- Article
- Local control of dopamine release in nucleus accumbens gates opioid withdrawal aversion.bioRxiv : the preprint server for biology · 2026Article
- Temporal single-cell atlas of full-length Huntington's disease mouse model defines stage-specific signatures of corticostriatal dysfunction.Molecular neurodegeneration · 2026Article
- Comparative analysis of the cellular landscape in mammalian striatum.Nature communications · 2026Article
- Region-specific transcriptional signatures of brain aging in the absence of neuropathology at the single-cell level.npj aging · 2026Article
- Double strand breaks drive toxicity in a Huntington's disease mouse model with or without somatic expansion.Nature communications · 2026Article
- Insights into neurodevelopmental features of Huntington's disease from stem cell-derived models including organoids.Journal of Huntington's disease · 2026Review
- Profiles of patients at early stages of Huntington's disease based on the routine biological markers and the disease progression.Journal of neurology · 2026Article
- Axonopathy: mechanisms and potential therapeutic targets for neurodegenerative diseases.Translational neurodegeneration · 2026Review
- Inter-individual variation of cellular and gene-expression properties of the human striatum.bioRxiv : the preprint server for biology · 2026Article
- Decoding neurodegeneration one cell at a time.The Journal of clinical investigation · 2026Review
- Astrocyte heterogeneity and gliosis in Huntington's disease: Histopathological insights into striatal and white matter pathology.Histology and histopathology · 2026Review
- Temporal single-cell atlas of full-length Huntington's disease mouse model defines stage-specific signatures of corticostriatal dysfunction.bioRxiv : the preprint server for biology · 2026Article
- Surface-Engineered Precision Nano-Systems for Targeted Treatment of Huntington's Disease: A Review of Recent Advancements.International journal of nanomedicine · 2026Review
- Differential morphology and distribution of GFAP astrocytes in vocal brain circuit in a songbird Southern house wren and humans.Frontiers in neuroanatomy · 2026Article
- From diet to brain repair: natural bioactive compounds in post-ischemic stroke recovery.Frontiers in nutrition · 2026Review
- Surprises From the Basal Ganglia: Stop and Go Have New Meaning.Movement disorders : official journal of the Movement Disorder Society · 2025Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Striatal projection neurons (SPNs), which progressively degenerate in human patients with Huntington's disease (HD), are classified along two axes: the canonical direct-indirect pathway division and the striosome-matrix compartmentation. It is well established that the indirect-pathway SPNs are susceptible to neurodegeneration and transcriptomic disturbances, but less is known about how the striosome-matrix axis is compromised in HD in relation to the canonical axis. Here we show, using single-nucleus RNA-sequencing data from male Grade 1 HD patient post-mortem brain samples and male zQ175 and R6/2 mouse models, that the two axes are multiplexed and differentially compromised in HD. In human HD, striosomal indirect-pathway SPNs are the most depleted SPN population. In mouse HD models, the transcriptomic distinctiveness of striosome-matrix SPNs is diminished more than that of direct-indirect pathway SPNs. Furthermore, the loss of striosome-matrix distinction is more prominent within indirect-pathway SPNs. These results open the possibility that the canonical direct-indirect pathway and striosome-matrix compartments are differentially compromised in late and early stages of disease progression, respectively, differentially contributing to the symptoms, thus calling for distinct therapeutic strategies.
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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.