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Jang-Ho J. Cha

Researcher at Harvard University

Publications -  25
Citations -  4157

Jang-Ho J. Cha is an academic researcher from Harvard University. The author has contributed to research in topics: Huntingtin & Huntington's disease. The author has an hindex of 22, co-authored 25 publications receiving 4004 citations. Previous affiliations of Jang-Ho J. Cha include Merck & Co..

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Minocycline inhibits caspase-1 and caspase-3 expression and delays mortality in a transgenic mouse model of Huntington disease.

TL;DR: It is reported that minocycline delays disease progression, inhibits casp enzyme-1 and caspase-3 mRNA upregulation, and decreases inducible nitric oxide synthetase activity, in the R6/2 mouse model of Huntington disease.
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Inhibition of caspase-1 slows disease progression in a mouse model of Huntington's disease

TL;DR: Evidence of caspase-1 activation in the brains of mice and humans with Huntington's disease is demonstrated and it is demonstrated that intracerebroventricular administration of a casp enzyme inhibitor delays disease progression and mortality in the mouse model of Huntington’s disease.
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Altered brain neurotransmitter receptors in transgenic mice expressing a portion of an abnormal human Huntington disease gene

TL;DR: Analysis of glutamate receptors in symptomatic 12-week-old R6/2 mice revealed decreases compared with age-matched littermate controls in the type 1 metabotropic GluR, and in situ hybridization indicated that mGluR and D1 dopamine receptor mRNA were altered as early as 4 weeks of age, long prior to the onset of clinical symptoms.
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CaMKII: a biochemical bridge linking accumbens dopamine and glutamate systems in cocaine seeking.

TL;DR: It is shown that stimulation of D1-like dopamine receptors in the nucleus accumbens shell reinstates cocaine seeking by activating L-type Ca2+ channels and CaMKII, suggesting an essential link between accumben shell dopamine and glutamate systems involved in the neuronal plasticity underlying cocaine craving and relapse.
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Altered neurotransmitter receptor expression in transgenic mouse models of Huntington's disease

TL;DR: The results suggest that receptor decreases precede, and therefore might contribute to, the development of clinical symptoms, and altered transcription of specific genes might be a key pathological mechanism in HD.