ArticleBrain communications2023
Early detection of exon 1 huntingtin aggregation in zQ175 brains by molecular and histological approaches.
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Article in Brain communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23citing papers in PubMed
3.5field-weighted citation impact, top 6% of its field
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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- The HTT1a protein initiates HTT aggregation in a knock-in mouse model of Huntington's disease.Brain : a journal of neurology · 2026Article
- Human-specific sequence features in HTT exon 1 promote toxic misprocessing via splicing factor SRSF7.Nature communications · 2026Article
- Targeted quantification assays for DNA repair and handling proteins and interactions in Huntington's disease models.bioRxiv : the preprint server for biology · 2026Article
- Molecular features of a Huntington's disease knock-in minipig.Disease models & mechanisms · 2026Article
- Enhancing the detection of HTT1a with neoepitope antibodies in mouse models of Huntington's disease.Brain communications · 2026Article
- Suppression of Huntington's Disease Somatic Instability by Transcriptional Repression and Direct CAG Repeat Binding.Nature communications · 2025Article
- Development of cognitive, motor, metabolic, and mutant huntingtin aggregation in the zQ175 mouse model of Huntington's disease.Scientific reports · 2025Article
- Complex cognitive and motivational deficits precede motor dysfunction in the zQ175 (190 CAG repeat) Huntington's disease model.Experimental neurology · 2025Article
- Multi-epitope immunocapture of huntingtin reveals striatum-selective molecular signatures.Molecular systems biology · 2025Article
- Small molecule modulation of p75Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Accelerated epigenetic aging in Huntington's disease involves polycomb repressive complex 1.Nature communications · 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
- Ubiquitin specific peptidase 11 knockdown slows Huntington's disease progression via regulating mitochondrial dysfunction and neuronal damage depending on PTEN-mediated AKT pathway.Molecular medicine (Cambridge, Mass.) · 2025Article
- Mutant huntingtin exon 1 protein detected in mouse brain with neoepitope antibody: effects of CAG repeat expansion, MutS Homolog 3 silencing and aggregation.Brain communications · 2025Article
- Exon 1-targeting miRNA reduces the pathogenic exon 1 HTT protein in Huntington's disease models.Brain : a journal of neurology · 2024Article
- Developmental and physiological impacts of pathogenic human huntingtin protein in the nervous system.Neurobiology of disease · 2024Article
- Evolution of aberrant brain-wide spatiotemporal dynamics of resting-state networks in a Huntington's disease mouse model.Clinical and translational medicine · 2024Article
- A CAG repeat threshold for therapeutics targeting somatic instability in Huntington's disease.Brain : a journal of neurology · 2024Article
- Mutant huntingtin protein decreases with CAG repeat expansion: implications for therapeutics and bioassays.Brain communications · 2024Article
- Beneficial effects of miR-132/212 deficiency in the zQ175 mouse model of Huntington's disease.Frontiers in neuroscience · 2024Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 3 countries.
Edward J SmithHuntington's Disease Centre, Department of Neurodegenerative Disease and UK Dementia Research Institute at UCL, Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK.
Kirupa SathasivamHuntington's Disease Centre, Department of Neurodegenerative Disease and UK Dementia Research Institute at UCL, Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK.
Christian LandlesHuntington's Disease Centre, Department of Neurodegenerative Disease and UK Dementia Research Institute at UCL, Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK.ORCID https://orcid.org/0000-0001-9715-6447
Georgina F OsborneHuntington's Disease Centre, Department of Neurodegenerative Disease and UK Dementia Research Institute at UCL, Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK.ORCID https://orcid.org/0000-0001-8308-3179
Michael A MasonHuntington's Disease Centre, Department of Neurodegenerative Disease and UK Dementia Research Institute at UCL, Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK.
Casandra Gomez-ParedesHuntington's Disease Centre, Department of Neurodegenerative Disease and UK Dementia Research Institute at UCL, Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK.ORCID https://orcid.org/0000-0001-7477-4226
Bridget A TaxyHuntington's Disease Centre, Department of Neurodegenerative Disease and UK Dementia Research Institute at UCL, Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK.
Rebecca E MiltonHuntington's Disease Centre, Department of Neurodegenerative Disease and UK Dementia Research Institute at UCL, Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK.ORCID https://orcid.org/0000-0002-4373-1052
Anne AstNeuroproteomics, Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin 13125, Germany.
Franziska SchindlerNeuroproteomics, Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin 13125, Germany.ORCID https://orcid.org/0000-0002-3320-8284
Chuangchuang ZhangDivision of Neurobiology, Department Psychiatry and Behavioral Sciences; Department Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Wenzhen DuanDivision of Neurobiology, Department Psychiatry and Behavioral Sciences; Department Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.ORCID https://orcid.org/0000-0001-5933-6308
Erich E WankerNeuroproteomics, Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin 13125, Germany.
Gillian P BatesHuntington's Disease Centre, Department of Neurodegenerative Disease and UK Dementia Research Institute at UCL, Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK.ORCID https://orcid.org/0000-0002-4041-6305
UK Dementia Research Institute · GBMax Delbrück Center · DEJohns Hopkins University · US
Funding
Advanced MRI biomarkers in HD mouse models translatable to humans: nature history and response to therapeuticsR01NS124084 · NINDS · JOHNS HOPKINS UNIVERSITY · PI DUAN, WENZHEN · 2022 to 2025
$2.6MEmerging role of glymphatic clearance in Huntington's diseaseR01NS127344 · NINDS · JOHNS HOPKINS UNIVERSITY · PI Wenzhen Duan, JIadi Xu · 2023 to 2026
$2.0MImaging brain glucose uptake by onVDMP MRI in Huntington's DiseaseR21NS118079 · NINDS · JOHNS HOPKINS UNIVERSITY · PI DUAN, WENZHEN, XU, JIADI · 2020 to 2020
$465kNINDS NIH HHS R21 NS118079
Abstract
Huntingtin-lowering approaches that target huntingtin expression are a major focus for therapeutic intervention for Huntington's disease. When the cytosine, adenine and guanine repeat is expanded, the huntingtin pre-mRNA is alternatively processed to generate the full-length huntingtin and
Indexed as
HTTexon1huntingtin aggregationhuntingtin HTRF bioassayHuntington’s diseasezQ175 knock-in mouse model
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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.