MELAS 中海马区钙结合蛋白 D28K 表达减少与认知障碍。
Decreased hippocampal expression of calbindin D28K and cognitive impairment in MELAS.
机构信息
Department of Neurology, Columbia University Medical Center, New York, NY 10032, USA.
出版信息
J Neurol Sci. 2012 Jun 15;317(1-2):29-34. doi: 10.1016/j.jns.2012.03.005. Epub 2012 Apr 5.
Abstract
Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) is a maternally inherited mitochondrial syndrome characterized by seizures, migrainous headaches, lactic acidosis, vomiting, and recurrent stroke-like episodes. Patients often suffer from cognitive dysfunction of unclear pathogenesis. In this study, we explored a possible link between cognitive dysfunction and hippocampal expression of calbindin D(28KD) (CB), a high affinity calcium-binding protein, in four MELAS patients, using post mortem hippocampal tissues. We found significantly reduced CB levels in all patients by immunohistochemistry, Western blot, and quantitative real-time PCR. Reduction in CB expression has been associated with aging and with neurodegenerative disorders, including Alzheimer's disease. We postulate that the reduced CB expression may play a role in the cognitive abnormalities associated with MELAS.
摘要
线粒体脑肌病伴高乳酸血症和卒中样发作（MELAS）是一种母系遗传的线粒体综合征，其特征为癫痫发作、偏头痛、乳酸酸中毒、呕吐和反复卒中样发作。患者常伴有不明病因的认知功能障碍。在这项研究中，我们使用死后海马组织，探讨了认知功能障碍与钙结合蛋白 CB（calbindin D(28KD)）在 4 位 MELAS 患者海马表达之间的可能联系。免疫组织化学、Western blot 和定量实时 PCR 显示所有患者的 CB 水平均显著降低。CB 表达减少与衰老和神经退行性疾病有关，包括阿尔茨海默病。我们推测，CB 表达减少可能与 MELAS 相关的认知异常有关。
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2
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Hippocampus. 2012 May;22(5):1107-20. doi: 10.1002/hipo.20957. Epub 2011 May 31.
3
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4
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Arch Neurol. 2009 Jan;66(1):85-91. doi: 10.1001/archneurol.2008.526.
5
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Methods. 2008 Dec;46(4):274-80. doi: 10.1016/j.ymeth.2008.09.027. Epub 2008 Oct 16.
6
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Cogn Behav Neurol. 2007 Jun;20(2):83-92. doi: 10.1097/WNN.0b013e3180335faf.
7
Population prevalence of the MELAS A3243G mutation.MELAS A3243G突变的人群患病率。
Mitochondrion. 2007 May;7(3):230-3. doi: 10.1016/j.mito.2006.12.004. Epub 2007 Jan 8.
8
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Trends Neurosci. 2007 Apr;30(4):167-75. doi: 10.1016/j.tins.2007.01.007. Epub 2007 Feb 9.
9
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Nat Rev Neurosci. 2007 Jan;8(1):33-44. doi: 10.1038/nrn2040.
10
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J Inherit Metab Dis. 2006 Feb;29(1):86-91. doi: 10.1007/s10545-006-0148-8.
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