Glial Cell Derived Neurotrophic Factors and Alzheimer's Disease

Ambrish J. Patel, Colin Wickenden, Angela Jen, H.A.Rohan de Silva
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引用次数: 9

Abstract

In Alzheimer's disease the normal balance of metabolic pathways regulating trophic factors/cytokines is disrupted; local reduction may result in neurons being deprived of neurotrophic factors while an excess may initiate a cascade of interaction between glial cells and β-amyloid precursor protein metabolism thereby facilitating plaque formation. This paper briefly discusses the findings of our group on aspects ranging from cholinergic humoral and trophic factors to mechanisms underlying amyloidogenesis in Alzheimer's disease.

神经胶质细胞源性神经营养因子与阿尔茨海默病
在阿尔茨海默病中,调节营养因子/细胞因子的代谢途径的正常平衡被破坏;局部减少可能导致神经元被剥夺神经营养因子,而过量可能启动神经胶质细胞和β-淀粉样前体蛋白代谢之间的级联相互作用,从而促进斑块的形成。本文简要讨论了我们小组在阿尔茨海默病中从胆碱能、体液和营养因子到淀粉样蛋白形成机制等方面的发现。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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