Mitochondrial phenotype in minipig model transgenic for N-terminal part of human mutated huntingtin

0485169 - ÚŽFG 2018 CZ eng K - Konferenční příspěvek (tuzemská konf.)
Hansíková, H. - Rodinová, M. - Křížová, J. - Dosoudilová, Z. - Štufková, H. - Bohuslavová, Božena - Klíma, Jiří - Juhás, Štefan - Ellederová, Zdeňka - Motlík, Jan - Zeman, J.
Mitochondrial phenotype in minipig model transgenic for N-terminal part of human mutated huntingtin.
The 4th Animal Models of Neurodegenerative Diseases. Liběchov: ÚŽFG AV ČR, v. v. i., 2017, s. 27-28.
[Animal Models of Neurodegenerative Diseases /4./. Liblice (CZ), 22.10.2017-24.10.2017]
Grant CEP: GA MŠMT(CZ) LO1609; GA MŠMT 7F14308
Institucionální podpora: RVO:67985904
Klíčová slova: minipig model * Huntington´s disease
Obor OECD: Neurosciences (including psychophysiology

Huntington’s disease (HD) is neurodegenerative disorder caused by an abnormal expansion of CAG repeat encoding a polyglutamine tract of huntingtin (htt). It has been postulated that mitochondria dysfunction may play significant role in the pathophysiology of the HD. But it is still not known yet in detail how mitochondria are able to cover energy needs of the cells during the progression of the HD.
Trvalý link: http://hdl.handle.net/11104/0280242