摘要
The cellular messenger nitric oxide（NO） has been linked to neurodegenerative disorders due to the increased expression of the enzymes that catalyze its synthesis in postmortem tissues derived from sufferers of these diseases.Nitrated proteins have also been detected in these samples,revealing that NO is biologically active in regions damaged during neurodegeneration.Modulation of NO levels has been reported not only in the neurons of the central nervous system,but also in the glial cells（microglia and astroglia） activated during the neuroinflammatory response.Neuroinflammation has been found in some neurodegenerative conditions,and inhibition of these neuroinflammatory signals has been shown to delay the progress of such disorders.Thus NO and the pathways triggering its release are emerging as an important research focus in the search for strategies to prevent,halt or cure neurodegenerative diseases.
一氧化氮(nitric oxide, NO)是一类胞内信使。研究表明,神经退行性病人脑组织中催化合成NO的酶的表达水平显著提高,提示NO与神经退行性疾病密切相关。此外,在这些组织中还检测到硝化的蛋白,提示NO在这些组织中具有生物活性。在神经免疫应答中,神经元和胶质细胞(包括小胶质细胞和星形胶质细胞)内都发生了NO水平的改变。很多神经退行性疾病都伴随有神经炎症,抑制神经炎症的信号通路能延迟这些疾病的发展。因此,NO及其释放通路已逐渐成为神经退行性疾病研究领域的热点,对它们的理解能帮助我们找到合适的方案来预防、减缓或者治愈这些疾病。
基金
supported by an Alzheimer's Society Personal Research Fellowship (93) with support from the Henry Smith Charity
Alzheimer's Society is a charity (registration no. 296645)
a company registered in England and Wales (registration no.2115499)
The University of St Andrews is a charity registered in Scotland (registration no. SC013532)
