ReviewJournal of neurochemistry2010
Differential vulnerability of neurons in Huntington's disease: the role of cell type-specific features.
Review in Journal of neurochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
97 citing papers in PubMed.
- iPSC Neurodegenerative Disease Initiative isogenic CAG repeat iPSC line for Huntington's disease.bioRxiv : the preprint server for biology · 2026Article
- Article
- DNA methylation profiling in Huntington's disease reveals disease associated changes in the striatum.Clinical epigenetics · 2026Article
- Inter-individual variation of cellular and gene-expression properties of the human striatum.bioRxiv : the preprint server for biology · 2026Article
- Mutant huntingtin expression in somatostatin-positive interneurons contributes to neurophysiological and behavioral phenotypes in BACHD mice.Disease models & mechanisms · 2026Article
- Cerebrospinal Fluid Proenkephalin Predicts Striatal Atrophy Decades before Clinical Motor Diagnosis in Huntington's Disease.Movement disorders : official journal of the Movement Disorder Society · 2026Article
- A shared DNA-repeat toxicity threshold, reached somatically at cell-type-specific rates, unites cortical and striatal neurodegeneration in Huntington's disease.bioRxiv : the preprint server for biology · 2025Article
- Post-Translational Modifications of Huntingtin: Mechanistic Insights and Therapeutic Opportunities in Huntington's Disease.International journal of molecular sciences · 2025Review
- 3D cultured human medium spiny neurons functionally integrate and rescue motor deficits in Huntington's disease mice.The Journal of clinical investigation · 2025Article
- CoREST in pieces: Dismantling the CoREST complex for cancer therapy and beyond.Science advances · 2025Review
- Autonomic dysfunction in neurodegenerative disease.Nature reviews. Neuroscience · 2025Review
- Examination of Anti-Inflammatory Effects After Propionate Supplementation in the R6/2 Mouse Model of Huntington's Disease.International journal of molecular sciences · 2025Article
- Absence of hippocampal pathology persists in the Q175DN mouse model of Huntington's disease despite elevated HTT aggregation.Journal of Huntington's disease · 2025Article
- New MiniPromoter Ple389 (ADORA2A) drives selective expression in medium spiny neurons in mice and non-human primates.Scientific reports · 2024Article
- Pathologic TDP-43 downregulates myelin gene expression in the monkey brain.Brain pathology (Zurich, Switzerland) · 2024Article
- Break-up and recovery of harmony between direct and indirect pathways in the basal ganglia: Huntington's disease and treatment.Cognitive neurodynamics · 2024Article
- Toxic effects of mutant huntingtin in axons are mediated by its proline-rich domain.Brain : a journal of neurology · 2024Article
- TYROBP/DAP12 knockout in Huntington's disease Q175 mice cell-autonomously decreases microglial expression of disease-associated genes and non-cell-autonomously mitigates astrogliosis and motor deterioration.Journal of neuroinflammation · 2024Article
- Cell type specification and diversity in subpallial organoids.Frontiers in genetics · 2024Review
- Live Imaging Analysis of Axonal Regeneration in Human iPSC-Derived Motor Neurons Using a Microfluidic System.Methods in molecular biology (Clifton, N.J.) · 2024Article
37 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Abnormal expansion of a polyglutamine tract in huntingtin (Htt) protein results in Huntington's disease (HD), an autosomal dominant neurodegenerative disorder involving progressive loss of motor and cognitive function. Contrasting with the ubiquitous tissue expression of polyglutamine-expanded Htt, HD pathology is characterized by the increased vulnerability of specific neuronal populations within the striatum and the cerebral cortex. Morphological, biochemical, and functional characteristics of neurons affected in HD that might render these cells more vulnerable to the toxic effects of polyglutamine-Htt are covered in this review. The differential vulnerability of neurons observed in HD is discussed in the context of various major pathogenic mechanisms proposed to date, and in line with evidence showing a 'dying-back' pattern of degeneration in affected neuronal populations.
Indexed as
Identifiers
What OpenQuestion holds
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.