ReviewMovement disorders : official journal of the Movement Disorder Society2014
Prospects for neuroprotective therapies in prodromal Huntington's disease.
Review in Movement disorders : official journal of the Movement Disorder Society, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 40 citations in OpenAlex.
- Planning for Prevention of Parkinson Disease: Now Is the Time.Neurology · 2022Article
- Utility of the Huntington's Disease Prognostic Index Score for a Perimanifest Clinical Trial.Movement disorders : official journal of the Movement Disorder Society · 2022Article
- Reactive Species in Huntington Disease: Are They Really the Radicals You Want to Catch?Antioxidants (Basel, Switzerland) · 2020Review
- Elucidating Critical Proteinopathic Mechanisms and Potential Drug Targets in Neurodegeneration.Cellular and molecular neurobiology · 2020Review
- Erucic acid, a nutritional PPARδ-ligand may influence Huntington's disease pathogenesis.Metabolic brain disease · 2020Review
- PGC-1α, Sirtuins and PARPs in Huntington's Disease and Other Neurodegenerative Conditions: NAD+ to Rule Them All.Neurochemical research · 2019Review
- Neurotheranostics as personalized medicines.Advanced drug delivery reviews · 2019Review
- Therapeutic approaches to Huntington disease: from the bench to the clinic.Nature reviews. Drug discovery · 2018Review
- Preclinical progression of neurodegenerative diseases.Nagoya journal of medical science · 2018Review
- Predictive testing and clinical trials in Huntington's disease: An ethical analysis.Movement disorders : official journal of the Movement Disorder Society · 2018Article
- Mitochondrial Dysfunction and Biogenesis in Neurodegenerative diseases: Pathogenesis and Treatment.CNS neuroscience & therapeutics · 2017Review
- The chicken or the egg: mitochondrial dysfunction as a cause or consequence of toxicity in Huntington's disease.Mechanisms of ageing and development · 2017Review
- Impaired muscle uptake of creatine in spinal and bulbar muscular atrophy.Annals of clinical and translational neurology · 2016Article
- Enhanced mitochondrial biogenesis ameliorates disease phenotype in a full-length mouse model of Huntington's disease.Human molecular genetics · 2016Article
- Laser Evoked Potentials in Early and Presymptomatic Huntington's Disease.Behavioural neurology · 2016Article
- [Huntington's disease].Der Nervenarzt · 2015Review
- A common gene expression signature in Huntington's disease patient brain regions.BMC medical genomics · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Huntington's disease (HD) is a prototypical dominantly inherited neurodegenerative disorder characterized by progressive cognitive deterioration, psychiatric disturbances, and a movement disorder. The genetic cause of the illness is a CAG repeat expansion in the huntingtin gene, which leads to a polyglutamine expansion in the huntingtin protein. The exact mechanism by which mutant huntingtin causes HD is unknown, but it causes abnormalities in gene transcription as well as both mitochondrial dysfunction and oxidative damage. Because the penetrance of HD is complete with CAG repeats greater than 39, patients can be diagnosed well before disease onset with genetic testing. Longitudinal studies of HD patients before disease onset have shown that subtle cognitive and motor deficits occur as much as 10 years before onset, as do reductions in glucose utilization and striatal atrophy. An increase in inflammation, as shown by elevated interleukin-6, occurs approximately 15 years before onset. Detection of these abnormalities may be useful in defining an optimal time for disease intervention to try to slow or halt the degenerative process. Although reducing gene expression with small interfering RNA or short hairpin RNA is an attractive approach, other approaches targeting energy metabolism, inflammation, and oxidative damage may be more easily and rapidly moved into the clinic. The recent PREQUEL study of coenzyme Q10 in presymptomatic gene carriers showed the feasibility of carrying out clinical trials to slow or halt onset of HD. We review both the earliest detectable clinical and laboratory manifestations of HD, as well as potential neuroprotective therapies that could be utilized in presymptomatic HD.
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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.