Title page for etd-0216112-112117


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URN etd-0216112-112117
Author Chueh-Tan Chen
Author's Email Address chuehtan@hotmail.com
Statistics This thesis had been viewed 5575 times. Download 982 times.
Department Biological Sciences
Year 2011
Semester 1
Degree Master
Type of Document
Language zh-TW.Big5 Chinese
Title The Possible Role of Neuron Autophagy on Amyloidogenesis Disorderswith Lead Exposure
Date of Defense 2012-01-09
Page Count 79
Keyword
  • Alzheimer’s Disease
  • amyloid precursor protein
  • autophagy
  • amyloidogensis disorders
  • apoptosis
  • β-amyloid protein
  • lead exposure
  • Abstract Lead (Pb) is one of the most well known toxic heavy metals in human beings and animals, which leads to toxic neurological disorders, cognitive problems, learning and memory disabilities. Epidemiological studies revealed that chronic lead exposure is one of the environmental risk factors which may cause Alzheimer’s Disease, which were speculated for the observation of cellular necrosis, apoptosis, and β-amyloid deposition frequently occuring altogether after chronic lead exposure. Recent studies have shown that the β-amyloid formed during autophagic turnover of APP-rich organelles supplied by both autophagy and endocytosis. Therefore, we will conduct the new perspective for studying the possible role of autophagy on amyloidogensis disorders after lead exposure. SH-SY5Y human neuroblastoma cells, used in this study, were differentiated to a neuronal phenotype by retinoic acid (RA) to the culture medium at 10 μM for 1, 2, 3 and 4 days. Doses of lead acetate with of lead acetate were 5 μM and applied to the neuronal culture and then cell viability measurement by MTT assay. The apoptotic effect of non-differentiation and differentiation neuroblastoma cells after lead exposure was determined by cleaved DNA fragments. Furthermore, APP, intracellular Aβ1-40 and Aβ1-42 expression were quantified by Real-time PCR and ELISA, respectively. The autophagy process and variation of total and phosphorylated mammalian target of rapamycin (mTOR) forms were determined after lead exposure in non-differentiation and differentiation neuroblastoma cells by western blot. The results indicate that lead exposure enhances autophagy response in both non-differentiation and differentiation SH-SY5Y cells, which might cause neuronal apoptosis associated with β-amyloidgenesis. Otherwise, lead exposure resulted in the inhibition of mTOR signaling, which correlated with the autophagic process. Besides, in our studies, non-differentiated cells exhibited more toxic vulnerability than RA induced differentiated neuron is congruous to previous finding that lead exposure during fetal development might be a potential risk factor for AD in the adulthood.
    Advisory Committee
  • Tai,Ming-Hong - chair
  • Chen,Tsan-Ju - co-chair
  • Cheng, Jiin-Tsuey - advisor
  • Chen, Shun-Sheng - advisor
  • Files
  • etd-0216112-112117.pdf
  • Indicate in-campus at 5 year and off-campus access at 5 year.
    Date of Submission 2012-02-16

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