Corticosterone dysregulation exacerbates disease progression in the R6/2 transgenic mouse model of Huntington's disease

Brett D. Dufour, Jodi McBride

    Research output: Contribution to journalArticle

    7 Scopus citations

    Abstract

    Huntington's disease (HD) is a genetic neurological disorder that causes severe and progressive motor, cognitive, psychiatric, and metabolic symptoms. There is a robust, significant elevation in circulating levels of the stress hormone, cortisol, in HD patients; however, the causes and consequences of this elevation are largely uncharacterized. Here, we evaluated whether elevated levels of corticosterone, the rodent homolog of cortisol, contributed to the development of symptomology in transgenic HD mice. Wild-type (WT) and transgenic R6/2 mice were given either 1) adrenalectomy with WT-level corticosterone replacement (10 ng/ml), 2) adrenalectomy with high HD-level corticosterone replacement (60 ng/ml), or 3) sham surgery without replacement. R6/2 mice on HD-level replacement showed severe and rapid weight loss (p 

    Original languageEnglish (US)
    Pages (from-to)308-317
    Number of pages10
    JournalExperimental Neurology
    Volume283
    DOIs
    StatePublished - Sep 1 2016

    Keywords

    • Circadian dysfunction
    • Corticosterone
    • Cortisol
    • HPA-axis
    • Huntington's disease
    • R6/2 transgenic mice

    ASJC Scopus subject areas

    • Neurology
    • Developmental Neuroscience

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