ReviewNeuroscience bulletin2022
CRISPR-Based Genome-Editing Tools for Huntington's Disease Research and Therapy.
Review in Neuroscience bulletin, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed.
- CRISPR-Cas9-based therapies for Huntington's disease and Friedreich's ataxia: mechanisms, advances, and future perspectives.Neurogenetics · 2026Review
- Integrating CRISPR/Cas technology with clinical trials: Principles, progress and challenges.Asian journal of pharmaceutical sciences · 2025Review
- CRISPR-based gene therapy for huntington's disease: current advances and future prospects.Neurogenetics · 2025Review
- Review
- Huntington's chorea: emerging fields in therapeutics (Review).Neurogenetics · 2025Review
- 3D Genome Architecture in Stem Cell Lineage Commitment: from Structural Organization to Precision Regulation.Advanced genetics (Hoboken, N.J.) · 2025Review
- Bridge RNA-Guided Genetic Recombination Tools for Treating Neurodegenerative Nucleotide Repeat Disorders.Neuroscience bulletin · 2025Article
- VDGE: a data repository of variation database for gene-edited animals across multiple species.Nucleic acids research · 2025Article
- CRISPR-Cas technologies in neurodegenerative disorders: mechanistic insights, therapeutic potential, and translational challenges.Frontiers in neurology · 2025Review
- HAP40 modulates mutant Huntingtin aggregation and toxicity in Huntington's disease mice.Cell death & disease · 2024Article
- CRISPR/Cas9 system and its applications in nervous system diseases.Genes & diseases · 2024Review
- REDOX Balance in Oligodendrocytes Is Important for Zebrafish Visual System Regeneration.Antioxidants (Basel, Switzerland) · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease (HD) is an autosomal dominantly-inherited neurodegenerative disease, which is caused by CAG trinucleotide expansion in exon 1 of the Huntingtin (HTT) gene. Although HD is a rare disease, its monogenic nature makes it an ideal model in which to understand pathogenic mechanisms and to develop therapeutic strategies for neurodegenerative diseases. Clustered regularly-interspaced short palindromic repeats (CRISPR) is the latest technology for genome editing. Being simple to use and highly efficient, CRISPR-based genome-editing tools are rapidly gaining popularity in biomedical research and opening up new avenues for disease treatment. Here, we review the development of CRISPR-based genome-editing tools and their applications in HD research to offer a translational perspective on advancing the genome-editing technology to HD treatment.
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.