Corticosterone dysregulation exacerbates disease progression in the R6/2 transgenic mouse model of Huntington's disease
作者： Brett D. Dufour , Jodi L. McBride
DOI: 10.1016/J.EXPNEUROL.2016.06.028
关键词: Endocrinology 、 Adrenalectomy 、 Transgene 、 Neurological disorder 、 Corticosterone 、 Hydrocortisone 、 Internal medicine 、 Genetically modified mouse 、 Disease 、 Huntington's disease 、 Medicine
摘要: Abstract Huntington's disease (HD) is a genetic neurological disorder that causes severe and progressive motor, cognitive, psychiatric, metabolic symptoms. There robust, significant elevation in circulating levels of the stress hormone, cortisol, HD patients; however, consequences this are largely uncharacterized. Here, we evaluated whether elevated corticosterone, rodent homolog contributed to development symptomology transgenic mice. Wild-type (WT) R6/2 mice were given either 1) adrenalectomy with WT-level corticosterone replacement (10 ng/ml), 2) high HD-level (60 ng/ml), or 3) sham surgery without replacement. on showed rapid weight loss (p
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