Ishihara Keiichi
Department of Pathological Biochemistry, Kyoto Pharmaceutical University, 5 Misasagi Nakauchi-cho, Yamashina-ku, Kyoto 607-8414, Japan.
J Clin Biochem Nutr. 2022 Jul;71(1):16-21. doi: 10.3164/jcbn.21-155. Epub 2022 Feb 15.
Individuals with Down syndrome (DS), which is caused by triplication of human chromosome 21 (Hsa21), show numerous characteristic symptoms, such as intellectual disability, an impaired cognitive function, and accelerated aging-like phenotypes. Enhanced oxidative stress is assumed to be implicated as a mechanism underlying many of these symptoms of DS. Some genes coded in Hsa21, such as , , and , are suggested as being involved in the exacerbation of oxidative stress. In addition, enhanced oxidative stress has been recently shown to be caused by dyshomeostasis of the redox-active bio-metal copper in the brain of a mouse model of DS. This review aims to summarize the current knowledge on enhanced oxidative stress in DS and suggest a possible molecular mechanism underlying the cognitive impairment of DS mediated by enhanced oxidative stress.
唐氏综合征(DS)由人类21号染色体(Hsa21)三体性引起,患者表现出许多特征性症状,如智力残疾、认知功能受损和加速衰老样表型。氧化应激增强被认为是DS许多这些症状的潜在机制。Hsa21编码的一些基因,如 、 和 ,被认为与氧化应激的加剧有关。此外,最近研究表明,氧化应激增强是由DS小鼠模型大脑中具有氧化还原活性的生物金属铜的动态失衡引起的。本综述旨在总结目前关于DS中氧化应激增强的知识,并提出氧化应激增强介导DS认知障碍的可能分子机制。