scholarly journals Hypothalamic expression of huntingtin causes distinct metabolic changes in Huntington’s disease mice

2022 ◽  
pp. 101439
Author(s):  
Elna Dickson ◽  
Rana Soylu-Kucharz ◽  
Åsa Petersén ◽  
Maria Björkqvist
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Metabolic Changes

scholarly journals Metabolic changes in the basal ganglia of patients with Huntington's disease: an insitu hybridization study of cytochrome oxidase subunitI mRNA

2002 ◽  
Vol 80 (3) ◽  
pp. 466-476 ◽  
Author(s):  
Isabelle Gourfinkel-An ◽  
Miquel Vila ◽  
Baptiste Faucheux ◽  
Charles Duyckaerts ◽  
Francois Viallet ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Cytochrome Oxidase ◽  
Metabolic Changes ◽  
Hybridization Study ◽  
Insitu Hybridization

A25 Psychiatric and metabolic changes in the BACHD mouse model of Huntington's disease

2010 ◽  
Vol 81 (Suppl 1) ◽  
pp. A8.2-A8
Author(s):  
S Hult ◽  
R Soylu ◽  
D Kirik ◽  
Å Petersén
Keyword(s):  
Mouse Model ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Metabolic Changes

scholarly journals IKKβ signaling mediates metabolic changes in the hypothalamus of a Huntington's disease mouse model

2021 ◽  
Author(s):  
Rana Soylu Kucharz ◽  
Ali Khoshnan ◽  
Asa Petersen
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Viral Vectors ◽  
Neurodegenerative Disorder ◽  
Metabolic Changes ◽  
Cag Repeat ◽  
Central Inhibition ◽  
Metabolic Imbalance ◽  
Obese Phenotype ◽  
Underlying Mechanisms

Background: Huntington's disease (HD) is a neurodegenerative disorder caused by a CAG repeat expansion in the huntingtin (HTT) gene. Metabolic changes are associated with HD progression, and underlying mechanisms are not fully known. As the IKKβ/NF-kB pathway is an essential regulator of metabolism, we investigated the involvement of IKKβ, the upstream activator of NF-kB in hypothalamus-specific HD metabolic changes. Methods: Using viral vectors, we expressed amyloidogenic N-terminal fragments of mutant HTT (mHTT) fragments in the hypothalamus of mice without IKKβ in the CNS (IKKβ-/-) and control mice (IKKβ+/+). We assessed effects on body weight, metabolic hormones, and hypothalamic neuropathology. Results: Hypothalamic expression of mHTT led to an obese phenotype only in female mice. CNS-specific inactivation of IKKβ prohibited weight gain in females, which was independent of neuroprotection and microglial activation. Conclusions: The expression of mHTT in the hypothalamus causes metabolic imbalance in a sex-specific fashion, and central inhibition of the IKKβ pathway attenuates the obese phenotype.

Memory Processes in Huntington's Disease

2007 ◽  
Author(s):  
John McDowall ◽  
Kristy Bolter
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Memory Processes
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