Molecular mechanisms of the aberrant metabolism of tryptophan in Alzheimer's disease

阿尔茨海默病(AD)是一种随着老年人口的增加而增加的神经退行性疾病。防治阿尔茨海默病是一个紧迫的社会问题。本研究通过吲哚胺2，3-双加氧酶的诱导，研究了色氨酸在AD中异常代谢的分子机制，从而产生神经毒素喹啉酸。尤其是淀粉样蛋白的假定受体。对活化的巨噬细胞表达的多肽渗入淀粉样斑块进行鉴定。

Alzheimer's disease(AD) is an increasing neurodegenerative disease with growing elderly population. Prevention and treatment of AD is an urgent social issue. In this study, molecular mechanisms of the aberrant metabolism of tryptophan via induction of indoleamine 2, 3-dioxygnase in AD, which leads to a generation of neurotoxin quinolinic acid, was studied. In particular, the putative receptor for amyloid. peptide expressed in activated macrophages infiltrating into amyloid plaques was tried to be characterized.