ArticleScientific reports2016
Metabolic and behavioral effects of mutant huntingtin deletion in Sim1 neurons in the BACHD mouse model of Huntington's disease.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 21 citations in OpenAlex.
- Aberrant medial ganglionic eminence (MGE) GABAergic neurogenesis contributes to Huntington's disease pathogenesis.Neurobiology of disease · 2026Article
- Hypothalamic expression of huntingtin causes distinct metabolic changes in Huntington's disease mice.Molecular metabolism · 2022Article
- IKKβ signaling mediates metabolic changes in the hypothalamus of a Huntington disease mouse model.iScience · 2022Article
- Oxytocin in Huntington's disease and the spectrum of amyotrophic lateral sclerosis-frontotemporal dementia.Frontiers in molecular neuroscience · 2022Review
- Effects of mutant huntingtin inactivation on Huntington disease-related behaviours in the BACHD mouse model.Neuropathology and applied neurobiology · 2021Article
- The Role of Hypothalamic Pathology for Non-Motor Features of Huntington's Disease.Journal of Huntington's disease · 2019Review
- Female Offspring From Chronic Hyperandrogenemic Dams Exhibit Delayed Puberty and Impaired Ovarian Reserve.Endocrinology · 2018Article
- Hypothalamic Alterations in Neurodegenerative Diseases and Their Relation to Abnormal Energy Metabolism.Frontiers in molecular neuroscience · 2018Review
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3 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Hypothalamic pathology, metabolic dysfunction and psychiatric symptoms are part of Huntington disease (HD), which is caused by an expanded CAG repeat in the huntingtin (HTT) gene. Inactivation of mutant HTT selectively in the hypothalamus prevents the development of metabolic dysfunction and depressive-like behavior in the BACHD mouse model. The hypothalamic paraventricular nucleus (PVN) is implicated in metabolic and emotional control, therefore we here tested whether inactivation of mutant HTT in the PVN affects metabolic and psychiatric manifestations of HD in BACHD mice. BACHD mice were crossed with mice expressing Cre-recombinase under the Sim1 promoter (Sim1-Cre) to inactivate mutant HTT in Sim1 expressing cells, i.e. the PVN of the hypothalamus. We found that inactivation of mutant HTT in Sim1 cells had a sex-specific effect on both the metabolic and the psychiatric phenotype, as these phenotypes were no longer different in male BACHD/Sim1-Cre mice compared to wild-type littermates. We also found a reduced number of GnRH neurons specifically in the anterior hypothalamus and an increased testes weight in male BACHD mice compared to wild-type littermates. Taken together, expression of mutant HTT in Sim1 cells may play a role for the development of metabolic dysfunction and depressive-like behavior in male BACHD mice.
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