See veebileht kasutab küpsiseid kasutaja sessiooni andmete hoidmiseks. Veebilehe kasutamisega nõustute ETISe kasutustingimustega. Loe rohkem
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"Mobilitas järeldoktori uurimistoetus (MJD)" projekt MJD35
MJD35 (MJD35) "Mitokondrite dünaamika neurodegeneratiivsete haiguste mudelites (1.09.2009−31.05.2014)", Michal Cagalinec, Tartu Ülikool, Tartu Ülikool, Arstiteaduskond.
MJD35
Mitokondrite dünaamika neurodegeneratiivsete haiguste mudelites
Mitochondrial Dynamics in Models of Neurodegenerative Diseases
1.09.2009
31.05.2014
Teadus- ja arendusprojekt
Mobilitas järeldoktori uurimistoetus (MJD)
ETIS klassifikaatorAlamvaldkondCERCS klassifikaatorFrascati Manual’i klassifikaatorProtsent
3. Terviseuuringud3.1. BiomeditsiinB470 Füsioloogia 3.1. Biomeditsiin (anatoomia, tsütoloogia, füsioloogia, geneetika, farmaatsia, farmakoloogia, kliiniline keemia, kliiniline mikrobioloogia, patoloogia)100,0
AsutusRollPeriood
Tartu Ülikoolkoordinaator01.09.2009−31.05.2014
Tartu Ülikool, Arstiteaduskondkoordinaator01.09.2009−31.05.2014
PerioodSumma
01.09.2014−31.05.20141 395 310,00 EEK (89 176,56 EUR)
89 176,56 EUR

Mitochondrial dysfunction is a common characteristic of all neurodegenerative diseases. However, the cause of this dysfunction has remained mystery. One of the emerging theories behind the causes of observed mitochondrial dysfunction has been related with mitochondrial dynamics. All major neurodegenerative diseases are associated with impaired motility and mitochondrial fragmentation, latter related with imbalance of fusion/ fission dynamics. However, current knowledge seems to be limited to say in what extent these two phenomena are related. Could impaired motility be behind observed mitochondrial shortening/fragmentation? Could mitochondrial fragmentation impair somehow mitochondrial motility? Which of these factors is responsible for observed local/global energetic deficit? With the present project I present a hypothesis that changes in mitochondrial motility are leading to decreased mitochondrial fusion rate that in turn results in mitochondrial shortening or fragmentation. I also suggest that mitochondrial fragmentation together with impaired motility rather than altered fusion. rate are direct reasons for bioenergetic deficit resulting to axonal degeneration and neurodegeneration more general.