ReviewThe Yale journal of biology and medicine2013
Huntington's disease: the past, present, and future search for disease modifiers.
Review in The Yale journal of biology and medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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
19 citing papers in PubMed, 35 citations in OpenAlex.
- A retrospective analysis of hand tapping as a longitudinal marker of disease progression in Huntington's disease.BMC neurology · 2014Trial
- The effects of dual-task cognitive interference on gait and turning in Huntington's disease.PloS one · 2020Article
- A Combinatorial Cell and Drug Delivery Strategy for Huntington's Disease Using Pharmacologically Active Microcarriers and RNAi Neuronally-Committed Mesenchymal Stromal Cells.Pharmaceutics · 2019Article
- Time-effect relationship of acupuncture on histopathology, ultrastructure, and neuroethology in the acute phase of cerebral hemorrhage.Neural regeneration research · 2019Article
- The folding equilibrium of huntingtin exon 1 monomer depends on its polyglutamine tract.The Journal of biological chemistry · 2018Article
- Metformin reverses early cortical network dysfunction and behavior changes in Huntington's disease.eLife · 2018Article
- A novel ex vivo Huntington's disease model for studying GABAergic neurons and cell grafts by laser microdissection.PloS one · 2018Article
- Connecting Neuronal Cell Protective Pathways and Drug Combinations in a Huntington's Disease Model through the Application of Quantitative Systems Pharmacology.Scientific reports · 2017Article
- Huntingtin polyQ Mutation Impairs the 17β-Estradiol/Neuroglobin Pathway Devoted to Neuron Survival.Molecular neurobiology · 2017Article
- Neuroprotective effects of intrastriatal injection of rapamycin in a mouse model of excitotoxicity induced by quinolinic acid.Journal of neuroinflammation · 2017Article
- Article
- PIN1 Modulates Huntingtin Levels and Aggregate Accumulation: AnFrontiers in cellular neuroscience · 2017Article
- Role of NMDA Receptor-Mediated Glutamatergic Signaling in Chronic and Acute Neuropathologies.Neural plasticity · 2016Review
- Clinical Trials in a Dish: The Potential of Pluripotent Stem Cells to Develop Therapies for Neurodegenerative Diseases.Annual review of pharmacology and toxicology · 2016Review
- Structural Mechanisms of Mutant Huntingtin Aggregation Suppression by the Synthetic Chaperonin-like CCT5 Complex Explained by Cryoelectron Tomography.The Journal of biological chemistry · 2015Article
- Role of intestinal microbiota in the generation of polyphenol-derived phenolic acid mediated attenuation of Alzheimer's disease β-amyloid oligomerization.Molecular nutrition & food research · 2015Article
- Biochemical characterization of mutants in chaperonin proteins CCT4 and CCT5 associated with hereditary sensory neuropathy.The Journal of biological chemistry · 2014Article
- Microtubule-stabilizing agents as potential therapeutics for neurodegenerative disease.Bioorganic & medicinal chemistry · 2014Review
- Small non-coding RNAs add complexity to the RNA pathogenic mechanisms in trinucleotide repeat expansion diseases.Frontiers in molecular neuroscience · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease (HD) is an autosomal dominant genetic disorder that specifically causes neurodegeneration of striatal neurons, resulting in a triad of symptoms that includes emotional, cognitive, and motor disturbances. The HD mutation causes a polyglutamine repeat expansion within the N-terminal of the huntingtin (Htt) protein. This expansion causes aggregate formation within the cytosol and nucleus due to the presence of misfolded mutant Htt, as well as altered interactions with Htt's multiple binding partners, and changes in post-translational Htt modifications. The present review charts efforts toward a therapy that delays age of onset or slows symptom progression in patients affected by HD, as there is currently no effective treatment. Although silencing Htt expression appears promising as a disease modifying treatment, it should be attempted with caution in light of Htt's essential roles in neural maintenance and development. Other therapeutic targets include those that boost aggregate dissolution, target excitotoxicity and metabolic issues, and supplement growth factors.
Indexed as
Identifiers
23766742PMC3670441W1548964109What 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.