β-淀粉样蛋白和T淋巴细胞相互作用对神经元再生影响的初步分析-人体解剖与组织胚胎学专业论文.docxVIP

β-淀粉样蛋白和T淋巴细胞相互作用对神经元再生影响的初步分析-人体解剖与组织胚胎学专业论文.docx

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β-淀粉样蛋白和T淋巴细胞相互作用对神经元再生影响的初步分析-人体解剖与组织胚胎学专业论文

广东药学院硕士研究生学位论文 广东药学院硕士研究生学位论文 i i Preliminary study of the cross-talking effects of Amyloid-β and T lymphocytes on neurogenesis Meige Zheng (Human Anatomy and Histo-embryology) Supervisor: Prof.Guoying Li Abstract Background: Alzheimers disease (AD), a devastating neurodegenerative disease, is the most common form of dementia. Currently, the “amyloid hypothesis” is the most widely accepted explanation for the pathogenesis of AD. According to this hypothesis, amyloid-β (Aβ) peptide,the major component of senile plaques, is considered to play a crucial role in the pathological cascade invoved in the etiology of AD. Accumulation of Aβ in the specific encephalic region can lead to synaptic dysfunction, disrupting neural connectivity and neuronal death, which give rise to the clinical symptoms of AD, progressive loss of memory and cognitive impairment. Although the neurotoxicity of Aβ is widely accepted, whether it’s affecting neurogenesis is still unclear. In the current study, researchers have identified that CNS-specific T lymphocytes as being important to the maintenance of adult neurogenesis and spatial learning abilities. In addition, a number of reports suggest that T lymphocytes are activated in AD patients, and that these cells exist both in periphery and as infiltrates in the brain. However, the role of the infiltrating T cells in the AD process is still unknown. In order to investigate the roles of Aβ and T lymphocytes in AD, we take a sight of neurogenesis and postulate that: (1) In Alzheimer’s disease, not only can Aβ induce neuronal death, but inhibit neurogenesis, as causing a great quantity of neural loss and finally the pathogenesis of AD; (2) the toxic effects of Aβ that inhibit neurogenesis probably have an interaction with T lymphocytes which can promote neurogenesis, such as inhibiting the expression of key factors of T cells; (3) T lymphocytes can promote the clearance of Aβ to provide a beneficial milieu of the neurogenic niche for maintaining neu

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