| Summary: | 碩士 === 國立成功大學 === 臨床醫學研究所 === 101 === Frontotemporal lobar degeneration (FTLD) is a neurodegenerative disease which characterized by neuronal loss in frontal/temporal lobe of the brain. TAR DNA-binding protein-43 (TDP-43) was identified as the major component of the neurotoxic cytoplasmic and nuclear inclusions in brains of FTLD-U patients. Previous studies have revealed that gene dysregulation may be responsible for the pathogenesis of neurodegenerative diseases including FTLD. This thesis purposed to use CaMKII promoter-driven TDP-43 transgenic mice as FTLD mouse model to perform a global analysis of expressed genes and to elucidate novel genes involved in FTLD pathogenesis. In the comparison of gene-expression between FTLD mice and wild-type mice, transthyretin (TTR) was chosen as the candidate for further studies based on the correlations with neurodegenerative diseases. Expression level of TTR was upregulated in brains of FTLD mice. TTR was co-localized with TDP-43 inclusions and co-immunoprecipitated with TDP-43 in brains of FTLD mouse model. Taken together, TTR, which was upregulated in FTLD mice, interacted with TDP-43 and could play a role in FTLD pathogenesis.
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