## Abstract Phenocopies of Huntington's disease (HD) are individuals with a family history, clinical symptoms, and occasionally pathological evidence of HD but without an expanded CAG repeat within the HD gene. We report on an HD phenocopy with selective loss of preprotachykinin (PPT) neurons, dysf
Ginsenosides protect striatal neurons in a cellular model of Huntington's disease
β Scribed by Jun Wu; Hye Kyoung Jeong; Sarah Elizabeth Bulin; Sung Won Kwon; Jeong Hill Park; Ilya Bezprozvanny
- Publisher
- John Wiley and Sons
- Year
- 2009
- Tongue
- English
- Weight
- 311 KB
- Volume
- 87
- Category
- Article
- ISSN
- 0360-4012
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β¦ Synopsis
Abstract
Ginseng, the root of Panax ginseng C.A. Meyer (Araliaceae), is a widely used herbal medicine. Ginsenosides, the active ingredients of ginseng, are the main components responsible for many beneficial actions of ginseng. In the present study, we tested 10 different ginsenosides in the previously developed in vitro Huntington's disease (HD) assay with primary medium spiny striatal neuronal cultures (MSN) from the YAC128 HD mouse model. We found that nanomolar concentrations of ginsenoside Rb1 and Rc effectively protected YAC128 medium spiny neurons from glutamateβinduced apoptosis and that Rg5 was protective at micromolar concentration. The other seven ginsenosides tested were not effective or exerted toxic effects in MSN cultures. From further experiments, we suggested that neuroprotective effects of ginsenosides Rb1, Rc, and Rg5 could correlate with their ability to inhibit glutamateβinduced Ca^2+^ responses in cultured MSN. From these results we concluded that ginsenosides Rb1, Rc, and Rg5 offer a potential therapeutic choice for the treatment of HD and possibly other neurodegenerative disorders. Β© 2009 WileyβLiss, Inc.
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Differential loss of neurons and terminals occurs in Huntington's disease. Neurons expressing preproenkephalin (PPE) appear to be more vulnerable than neurons expressing preprotachykinin and terminals in the lateral pallidurn (containing enkephalin) are more affected than terminals in the medial pal
## Abstract Huntington's disease (HD) is a progressive neurodegenerative disorder caused by an expanded CAG repeat region in exon 1 of the HD gene. This mutation results in the presence of an abnormally long polyglutamine tract in the encoded protein, huntingtin (htt). A major question in this fiel