ReviewHistology and histopathology2008
Therapeutic perspectives for the treatment of Huntington's disease: treating the whole body.
Review in Histology and histopathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed.
- The Relaxin-3 Receptor, RXFP3, Is a Modulator of Aging-Related Disease.International journal of molecular sciences · 2022Review
- GPCRs Are Optimal Regulators of Complex Biological Systems and Orchestrate the Interface between Health and Disease.International journal of molecular sciences · 2021Review
- Therapeutic and Mechanistic Effects of Curcumin in Huntington's Disease.Current neuropharmacology · 2021Review
- Role of Mutant TBP in Regulation of Myogenesis on Muscle Satellite Cells.Current medical science · 2019Article
- 5΄-Vinylphosphonate improves tissue accumulation and efficacy of conjugated siRNAs in vivo.Nucleic acids research · 2017Article
- Partial Amelioration of Peripheral and Central Symptoms of Huntington's Disease via Modulation of Lipid Metabolism.Journal of Huntington's disease · 2016Article
- Article
- GIT2 Acts as a Systems-Level Coordinator of Neurometabolic Activity and Pathophysiological Aging.Frontiers in endocrinology · 2015Article
- Metabolic and hormonal signatures in pre-manifest and manifest Huntington's disease patients.Frontiers in physiology · 2014Article
- Possible involvement of self-defense mechanisms in the preferential vulnerability of the striatum in Huntington's disease.Frontiers in cellular neuroscience · 2014Review
- Systems-Level G Protein-Coupled Receptor Therapy Across a Neurodegenerative Continuum by the GLP-1 Receptor System.Frontiers in endocrinology · 2014Review
- Long-term artificial sweetener acesulfame potassium treatment alters neurometabolic functions in C57BL/6J mice.PloS one · 2013Article
- Euglycemic agent-mediated hypothalamic transcriptomic manipulation in the N171-82Q model of Huntington disease is related to their physiological efficacy.The Journal of biological chemistry · 2012Article
- Huntingtin aggregation kinetics and their pathological role in a Drosophila Huntington's disease model.Genetics · 2012Article
- Central role of the EGF receptor in neurometabolic aging.International journal of endocrinology · 2012Article
- Article
- GIT2 acts as a potential keystone protein in functional hypothalamic networks associated with age-related phenotypic changes in rats.PloS one · 2012Article
- Metabolic dysfunction in Alzheimer's disease and related neurodegenerative disorders.Current Alzheimer research · 2012Review
- Progressive and unconventional pharmacotherapeutic approaches to Alzheimer's disease therapy.Current Alzheimer research · 2012Article
- To be or not to be--obese.Endocrinology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Huntington's disease (HD) is a tremendously debilitating disorder that strikes relatively young individuals and progresses rapidly over the next ten to fifteen years inducing a loss of cognitive and motor skills and eventually death occurs. The primary locus of the disorder is a polyglutamine expansion of the protein product of the huntingtin (htt) gene. The htt protein appears to be a scaffolding protein that orchestrates the complex assembly of multiple intracellular proteins involved in multiple processes, including vesicular movement and cell metabolism. The htt protein is ubiquitously expressed in human tissues but the predominance of the interest in the pathology lies in its effects on the central nervous system (CNS). Most of the current therapeutics for HD thus have been targeted at preventing neuronal damage in the CNS, however, a considerable body of evidence has been accumulating to suggest that the maintenance of a healthy nervous system is tightly linked with peripheral physiological health. Therefore treatment of both the peripheral and central pathophysiologies of HD could form the basis of a more effective HD therapeutic strategy.
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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.