ReviewDrug design, development and therapy2015
Transgenic animal models for study of the pathogenesis of Huntington's disease and therapy.
Review in Drug design, development and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 59 citations in OpenAlex.
- Increased Activity-Dependent Bulk Endocytosis in Huntington's Disease Results From Huntingtin Haploinsufficiency.Journal of neurochemistry · 2025Article
- Deep behavioural phenotyping of the Q175 Huntington disease mouse model: effects of age, sex, and weight.BMC biology · 2024Article
- Nebulization of low-dose aspirin ameliorates Huntington's pathology in N171-82Q transgenic mice.NeuroImmune pharmacology and therapeutics · 2024Article
- Cannabinoid CB2 Receptors in Neurodegenerative Proteinopathies: New Insights and Therapeutic Potential.Biomedicines · 2022Review
- CAG Repeat Instability in the Peripheral and Central Nervous System of Transgenic Huntington's Disease Monkeys.Biomedicines · 2022Article
- Healthy Immunity on Preventive Medicine for Combating COVID-19.Nutrients · 2022Review
- TSPO imaging in animal models of brain diseases.European journal of nuclear medicine and molecular imaging · 2021Review
- Altered microRNA expression in animal models of Huntington's disease and potential therapeutic strategies.Neural regeneration research · 2021Review
- Understanding the brain uptake and permeability of small molecules through the BBB: A technical overview.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Review
- Translating CRISPR-Cas Therapeutics: Approaches and Challenges.The CRISPR journal · 2020Review
- The longevity-associated variant of BPIFB4 improves a CXCR4-mediated striatum-microglia crosstalk preventing disease progression in a mouse model of Huntington's disease.Cell death & disease · 2020Article
- Recent Overview of the Use of iPSCs Huntington's Disease Modeling and Therapy.International journal of molecular sciences · 2020Review
- In vitro modeling of the neurovascular unit: advances in the field.Fluids and barriers of the CNS · 2020Review
- Abnormal Brain Development in Huntington' Disease Is Recapitulated in the zQ175 Knock-In Mouse Model.Cerebral cortex communications · 2020Article
- Large Animal Models of Huntington's Disease: What We Have Learned and Where We Need to Go Next.Journal of Huntington's disease · 2020Review
- Stimulation of Sphingosine Kinase 1 (SPHK1) Is Beneficial in a Huntington's Disease Pre-clinical Model.Frontiers in molecular neuroscience · 2019Article
- HttQ111/+ Huntington's Disease Knock-in Mice Exhibit Brain Region-Specific Morphological Changes and Synaptic Dysfunction.Journal of Huntington's disease · 2018Article
- Impaired Performance of the Q175 Mouse Model of Huntington's Disease in the Touch Screen Paired Associates Learning Task.Frontiers in behavioral neuroscience · 2018Article
- Bridging the gap: large animal models in neurodegenerative research.Mammalian genome : official journal of the International Mammalian Genome Society · 2017Review
- Microglial Activation in the Pathogenesis of Huntington's Disease.Frontiers in aging neuroscience · 2017Review
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 at 3 institutions in 2 countries.
Funding
Abstract
Huntington's disease (HD) is caused by a genetic mutation that results in polyglutamine expansion in the N-terminal regions of huntingtin. As a result, this polyQ expansion leads to the misfolding and aggregation of mutant huntingtin as well as age-dependent neurodegeneration. The genetic mutation in HD allows for generating a variety of animal models that express different forms of mutant huntingtin and show differential pathology. Studies of these animal models have provided an important insight into the pathogenesis of HD. Mouse models of HD include transgenic mice, which express N-terminal or full-length mutant huntingtin ubiquitously or selectively in different cell types, and knock-in mice that express full-length mutant Htt at the endogenous level. Large animals, such as pig, sheep, and monkeys, have also been used to generate animal HD models. This review focuses on the different features of commonly used transgenic HD mouse models as well as transgenic large animal models of HD, and also discusses how to use them to identify potential therapeutics. Since HD shares many pathological features with other neurodegenerative diseases, identification of therapies for HD would also help to develop effective treatment for different neurodegenerative diseases that are also caused by protein misfolding and occur in an age-dependent manner.
Indexed as
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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.