Patel A J, Wickenden C, Jen A, de Silva H A
Department of Biochemistry, Charing Cross and Westminster Medical School, London.
Neurodegeneration. 1996 Dec;5(4):489-96. doi: 10.1006/neur.1996.0068.
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 beta-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.
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打破；局部减少可能导致神经元缺乏神经营养因子，而过量则可能引发胶质细胞与β-淀粉样前体蛋白代谢之间的一系列相互作用，从而促进斑块形成。本文简要讨论了我们小组在从胆碱能体液和营养因子到阿尔茨海默病中淀粉样蛋白生成机制等方面的研究结果。
