| Summary: | 碩士 === 國立陽明大學 === 解剖暨細胞生物學研究所 === 97 === Alzheimer's disease (AD) is the most common form of dementia in the aged persons. 5% of AD patients are familial heredity, other 95% of AD patients are sporadic, the late-onset case. The etiology of AD remains unclear. Oligomeric Abeta (oAbeta) appears prior to the senile plaque. The electricity physiological studies show that the long-term potentiation (LTP) of the hippocampus is reduced. The behavior studies show that the learning and memories in the presence of oAbeta reduced. It is shown that the peripheral inflammation on the prion transgenic mice will further deteriorate the prion-induced neurodegeneration. Therefore, my research hypothesis is that peripheral inflammation will accelerate the appearance of oAbeta during the pathology of AD. Based on the characterization of APP/PS1 double transgenic mice published in the literature, the minor Abeta plaque appears at 6.5 months. The systemic inflammation is induced in intraperitoneal injection 1.5 mg/kg LPS into 6.5 months old APP/PS1 transgenic mice. In this thesis, I explored the relationship between the systemic inflammation and the AD pathology development. After 6 weeks LPS injection, these mice were carried out the Morris water maze test. Afterward, some of control and LPS groups partial mice were sacrificed for Abeta senile plaque characterization. The rest mice were carry out the fear contextual test. Using the cue reference memory version of the Morris water maze test, the LPS group has longer latency than the saline group. Moreover, in fear contextual test, the LPS group has lower freezing percentage than the saline group of transgenic mice. It is suggested that peripheral LPS injection in APP/PS1 transgenic mice might cause the acquisition learning deficit. Because the pathological examination did not find any Abeta plaque at 9 month-old transgenic mice. The rest of transgenic mice at 11 months old were injected 5mg/kg LPS and sacrificed in 12 months old. Thioflavin-S and BSB were used to stain the characterization of beta-amyloid plaques. The morphology of beta-amyloid plaque in two groups of mice looks similar. The number of Abeta plaques in the saline group and the LPS group of APP/PS1 transgenic mice vary significantly. Only 3 out of 7 saline group and 2 out of 8 LPS group contain senile plaques. Due to the small number of Abeta plaque-carrying mice, the comparison of the area and number of ��-amyloid plaque in saline and LPS group of APP/PS1 transgenic mice are not further proceeded.
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