Evaluation of clinically relevant glutamate pathway inhibitors in in vitro model of Huntington's disease
@article{Wu2006EvaluationOC, title={Evaluation of clinically relevant glutamate pathway inhibitors in in vitro model of Huntington's disease}, author={Jun Wu and Tie-Shan Tang and Ilya B. Bezprozvanny}, journal={Neuroscience Letters}, year={2006}, volume={407}, pages={219-223} }
55 Citations
Neuroprotective Effect of EDR Peptide in Mouse Model of Huntington's Disease
- Biology, Chemistry
- 2017
The data obtained prompt EDR peptide capability to restore the morphology of spines in striatum neurons in Huntington’s disease (HD) mouse model and the proposed model suggests that E DR peptide binds specific binding site oligo (dCG) along the DNA minor groove.
Neuronal store-operated calcium entry pathway as a novel therapeutic target for Huntington's disease treatment.
- BiologyChemistry & biology
- 2011
Evaluation of Dimebon in cellular model of Huntington's disease
- BiologyMolecular Neurodegeneration
- 2008
The results suggest that Ca2+ and mitochondria stabilizing effects may, in part, be responsible for beneficial clinical effects of Dimebon.
Experimental models of HD and reflection on therapeutic strategies.
- BiologyInternational review of neurobiology
- 2011
Corticostriatal circuit dysfunction in Huntington's disease: intersection of glutamate, dopamine and calcium.
- BiologyFuture neurology
- 2010
The most current findings that implicate glutamate, dopamine and calcium signaling in this system and how they work in concert to disrupt corticostriatal function are summarized and therapeutic strategies related to altered corticOSTriatal signaling in HD are highlighted.
Dopaminergic Signaling and Striatal Neurodegeneration in Huntington's Disease
- BiologyThe Journal of Neuroscience
- 2007
The results suggest that dopamine signaling pathway plays an important role in HD pathogenesis and that antagonists of dopamine pathway such as tetrabenazine or dopamine receptor blockers may have a therapeutic potential for treatment of HD beyond well established “symptomatic” benefit.
Pathophysiology of Huntington's disease: from huntingtin functions to potential treatments
- Biology, ChemistryCurrent opinion in neurology
- 2008
Successful neuroprotective therapy for Huntington's disease patients is likely to involve a combined approach targeting both cellular and molecular mediators that account for the toxicity of mutated huntingtin.
A mitochondrial basis for Huntington’s disease: therapeutic prospects
- BiologyMolecular and Cellular Biochemistry
- 2013
Targeting mitochondria for their protection, while addressing symptomatic recovery, holds a great potential to tone down the progression of the disease, and to provide better relief to the patients and caretakers.
Novel targets for Huntington’s disease: future prospects
- Biology, PsychologyDegenerative neurological and neuromuscular disease
- 2016
The status of, and supporting evidence for, potential novel treatments of HD that are currently under development or have reached the level of early Phase I/II clinical trials are discussed.
Dantrolene is neuroprotective in Huntington's disease transgenic mouse model
- BiologyMolecular Neurodegeneration
- 2011
The hypothesis that deranged Ca2+ signaling plays an important role in HD pathology is supported and the RyanR inhibitors and Ca2- signaling stabilizers such as dantrolene should be considered as potential therapeutics for the treatment of HD and other polyQ-expansion disorders.
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