Tanji K, Schon E A, DiMauro S, Bonilla E
Department of Neurology, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA.
J Neurol Sci. 2000 Sep 1;178(1):29-36. doi: 10.1016/s0022-510x(00)00354-3.
Kearns-Sayre syndrome (KSS) is a sporadic multisystem disorder due to a defect of oxidative phosphorylation and associated with clonally-expanded rearrangements of mitochondrial DNA (mtDNA) deletions (Delta-mtDNAs) and/or duplications (dup-mtDNAs). To gain further insight into the pathogenesis of CNS dysfunction in KSS, we studied the choroid plexus from two autoptic cases using in situ hybridization (ISH) of mtDNA, and immunohistochemistry to detect mtDNA and nuclear DNA-encoded subunits of the respiratory chain. Neuropathological examination of both cases showed oncocytic transformation of choroid plexus epithelial cells. In the same cells, ISH demonstrated that the predominant species of mtDNA were Delta-mtDNAs, and immunohistochemistry showed a decreased expression of mtDNA-encoded proteins. We suggest that mitochondrial abnormalities due to the presence of abundant Delta-mtDNAs in the choroid plexus play an important role in causing the increased cerebrospinal fluid (CSF) protein and reduced folic-acid levels that are characteristic of KSS.
卡恩斯-塞尔综合征(KSS)是一种散发性多系统疾病,由氧化磷酸化缺陷引起,与线粒体DNA(mtDNA)缺失(Delta-mtDNAs)和/或重复(dup-mtDNAs)的克隆性扩增重排有关。为了进一步深入了解KSS中枢神经系统功能障碍的发病机制,我们使用mtDNA原位杂交(ISH)和免疫组织化学方法检测呼吸链的mtDNA和核DNA编码亚基,对两例尸检病例的脉络丛进行了研究。两例病例的神经病理学检查均显示脉络丛上皮细胞呈嗜酸性变。在同一细胞中,ISH显示mtDNA的主要类型是Delta-mtDNAs,免疫组织化学显示mtDNA编码蛋白的表达降低。我们认为,脉络丛中大量Delta-mtDNAs的存在导致的线粒体异常在引起KSS特征性的脑脊液(CSF)蛋白升高和叶酸水平降低方面起重要作用。