| Summary: | 碩士 === 慈濟大學 === 生理暨解剖醫學碩士班 === 99 === It has been demonstrated that PPARγ agonists reduce neuronal cell loss in in vitro
models of neurotoxicity and in in vivo models of Alzheimer's Disease, Parkinson’s
disease and amyotrophic lateral sclerosis. In this study, we treat rosiglitazone three
days in the first and then we treat rosiglitazone fifty-six days to investigate the neuron
cells’ morphology and whether it has neuroprotective effects. At last, we investigate
what PPARγ plays the neuroprotective role in neurodegenerative disease. In this study,
we also use Huntington's disease's (HD) transgenic mice model. HD is an autosomal
dominant hereditary neurodegenerative disease caused by a CAG trinucleotide repeats
exceptional expansion of exon 1 of the Huntingtin (Htt) gene. HD is due to brain
neurons continued to degenerate, resulting in nervous system signaling some areas
serious dysfunction. HD will attack the brain neurons, also particularly the cerebellum
and hippocampus specific. In the brain of the HD mice, the baseline levels of PPARγ
and mitochondrial genes (PGC-1α, NRF-1, NRF-2 and Tfam) mRNA were reduced
and then we use TZD treatment, PPARγ and mitochondrial genes (PGC-1α, NRF-1,
NRF-2 and Tfam) mRNA were recoverd. The baseline levels of Bcl-2, HSP-60,
HSP-70 proteins were also reduced in HD mice. We use TZD treatment also recoverd
in HD mice. Therefore, this study investigate the activation of PPARγ in HD mice
brain of mitochondrial function, which may be an important therapeutic approach to
improve brain damage in HD symptoms.
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