ArticleInternational journal of biomedical science : IJBS2011
Huntington's Disease: From Mutant Huntingtin Protein to Neurotrophic Factor Therapy.
Article in International journal of biomedical science : IJBS, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
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- Navigating triplet repeats sequencing: concepts, methodological challenges and perspective for Huntington's disease.Nucleic acids research · 2025Review
- Examining Balance and the Likelihood of Falls in Huntington's Disease.Clinical parkinsonism & related disorders · 2025Article
- Neurotrophins as Potential Gene Therapy Targets for Huntington's Disease.Current gene therapy · 2025Review
- Drosophila glial system: an approach towards understanding molecular complexity of neurodegenerative diseases.Molecular biology reports · 2024Review
- Palmitoylethanolamide, an endogenous fatty acid amide, and its pleiotropic health benefits: A narrative review.Journal of biomedical research · 2024Article
- Computational insights into missense mutations in HTT gene causing Huntington's disease and its interactome networks.Irish journal of medical science · 2023Article
- Functional Characterisation of the Circular RNA,Cells · 2023Article
- The Interaction ofCells · 2022Review
- The Kynurenine Pathway and Kynurenine 3-Monooxygenase Inhibitors.Molecules (Basel, Switzerland) · 2022Review
- Potential role of TrkB agonist in neuronal survival by promoting CREB/BDNF and PI3K/Akt signaling in vitro and in vivo model of 3-nitropropionic acid (3-NP)-induced neuronal death.Apoptosis : an international journal on programmed cell death · 2021Article
- Pharmaceutical and Nutraceutical Potential Applications ofBioMed research international · 2020Review
- Neurotheranostics as personalized medicines.Advanced drug delivery reviews · 2019Review
- Mutant Huntingtin Causes a Selective Decrease in the Expression of Synaptic Vesicle Protein 2C.Neuroscience bulletin · 2018Article
- Steroid and Xenobiotic Receptor Signalling in Apoptosis and Autophagy of the Nervous System.International journal of molecular sciences · 2017Review
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- Protein Glutathionylation in the Pathogenesis of Neurodegenerative Diseases.Oxidative medicine and cellular longevity · 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
1 author at 1 institution in 1 country.
Funding
Abstract
Huntington's disease (HD) is an inherited disorder characterized by neuronal dysfunction and degeneration in striatum and cerebral cortex. Although the signaling pathways involved in HD are not yet clearly elucidated, mutant huntingtin protein is a key factor in the induction of neurodegeneration. The mutant huntingtin protein alters intracellular Ca(2+) homeostasis, disrupts intracellular trafficking and impairs gene transcription. In this review, I emphasize the effects of mutant huntingtin protein in Ca(2+) handling and transcriptional factors. Transcriptional alterations are key factors in the deficits of several proteins involved in the cellular machinery. These proteins include neurotrophic factors such as brain-derived neurotrophic factor, fibroblast growth factor, glial-cell-line-derived neurotrophic factor, ciliary neurotrophic factor and neurturin that have been suggested to restore neuronal dysfunction, improve behavioral deficits and prolong the survival in animal models of HD. An understanding of the molecular pathways involved in neurodegeneration will shed light on the choice of neurotrophic factors targeting a specific neuronal population in HD and will consequently overcome behavioral deficits.
Identifiers
21841917PMC3154262W153224349What 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.