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代谢加工厂

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[资源] 从分子和代谢成像角度来看多发性硬化疾病的发病机制

来柳叶刀最新的一期杂志上看到一篇有关代谢成像的综述，在这儿跟大家分享一下（感兴趣的可以下载附件~~），题目为《Pathogenesis of multiple sclerosis: insights from molecular and metabolic imaging》，发表在Lancet Neurol. 2014 Jul 4. pii: S1474-4422(14)70101-2. doi: 10.1016/S1474-4422(14)70101-2.（http://www.thelancet.com/journals/laneur/article/PIIS1474-4422(14)70101-2/fulltext）
本篇新发表的文章阐述了与多发性硬化症导致复发与疾病渐进这些变化的发病机理。研究发现可以通过分子和代谢成像技术来探索临床前模型和患者的多发性硬化疾病机理。许多影像学研究表明：在没有损坏的血脑屏障情况下的持续炎症，在病灶内外激活了小神经胶质细胞，在急性病灶部位增加线粒体的活性，提高大脑中钠的浓度，也在急性病灶和正常呈现的脑白质中增加了谷氨酸盐的浓度，在不同的病人和病灶部位产生不同程度的髓鞘脱失，也对脑灰质造成早期神经元损伤以及脑白质和病灶的早期星形胶质细胞的增殖与活化。分子和代谢显像的技术推广和临床转化将使针对这些疾病的机制、新药的评估有了靶方向并能顺利展开，通过对患者进行分层治疗，会改善健康状况。（原文：The mechanisms underlying the pathogenesis of multiple sclerosis induce the changes that underpin relapseassociated and progressive disability. Disease mechanisms can be investigated in preclinical models and patients with multiple sclerosis by molecular and metabolic imaging techniques. Many insights have been gained from such imaging studies: persisting infl ammation in the absence of a damaged blood–brain barrier, activated microglia within and beyond lesions, increased mitochondrial activity after acute lesions, raised sodium concentrations in the brain, increased glutamate in acute lesions and normal-appearing white matter, diff erent degrees of demyelination in different patients and lesions, early neuronal damage in grey matter, and early astrocytic proliferation and activation in lesions and white matter. Clinical translation of molecular and metabolic imaging and extension of these techniques will enable the assessment of novel drugs targeted at these disease mechanisms, and have the potential to improve health outcomes through the stratifi cation of patients for treatments.）

p.s.另附代谢成像相关技术链接
《科学家发明细胞代谢成像新方法》（http://news.sciencenet.cn//htmlpaper/2011103110464332220238.shtm）（原英文 http://www.cell.com/cell-metabolism/abstract/S1550-4131(11)00350-0）（解读篇章 http://www.cutech.edu.cn/cn/kjjj/gwkj/2012/03/1331845686176961.htm）

在下不才，全在抛砖引玉，欢迎各位感兴趣的或者大牛们讨论交流~~

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