Euglycemic agent-mediated hypothalamic transcriptomic manipulation in the N171-82Q model of Huntington's disease is related to their physiological efficacy

ABSTRACT: Our aim was to find an effective treatment for the dysfunction in energy regulation and hypothalamic integrity occurring in many HuntingtonM-bM-^@M-^Ys disease (HD) patients and mouse models. HD is a neurodegenerative disease caused by an expanded CAG repeat and is characterized by mutant huntingtin aggregates, cell death, progressive motor impairment, and cognitive alterations. Changes in neuroendocrine function, body weight, energy metabolism, euglycemia, appetite function, sleep, and gut function can also occur. It is likely that the locus of these alterations is the hypothalamus. Male B6C3-Tg(HD82Gln)81Dbo/J (N171-82Q) mice and age-matched wild-type (WT) mice were used. Transgenic mice were identified by PCR analysis of tail DNA. N171-82Q mice express 82 polyglutamine repeats and displ

ORGANISM(S): Mus musculus

SUBMITTER: Kevin Becker 

PROVIDER: E-GEOD-39586 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress