نتایج جستجو برای: merzbacher

تعداد نتایج: 317  

2015
Teva Brender Donna Wallerstein John Sum Robert Wallerstein

Pelizaeus-Merzbacher disease (PMD) is neurodegenerative leukodystrophy caused by dysfunction of the proteolipid protein 1 (PLP1) gene on Xq22, which codes for an essential myelin protein. As an X-linked condition, PMD primarily affects males; however there have been a small number of affected females reported in the medical literature with a variety of different mutations in this gene. No affec...

Journal: :American journal of medical genetics 1995
V M Pratt S Boyadjiev S R Dlouhy K Silver V M Der Kaloustian M E Hodes

Single-strand conformational polymorphism analysis of an affected male with Pelizaeus-Merzbacher disease (PMD) showed a slight change in mobility of amplified exon 5 of the proteolipid protein (PLP) gene. The exon was sequenced and a G-->A transition at codon 216 was found. This mutation eliminates a BstNI restriction site and creates a MaeI restriction site. In 1989, Gencic et al. reported a m...

Journal: :Geografiska Annaler: Series A, Physical Geography 2008

2018
Haoran Ji Dongxiao Li Ye Wu Quanli Zhang Qiang Gu Han Xie Taoyun Ji Huifang Wang Lu Zhao Haijuan Zhao Yanling Yang Hongchun Feng Hui Xiong Jinhua Ji Zhixian Yang Liping Kou Ming Li Xinhua Bao Xingzhi Chang Yuehua Zhang Li Li Huijuan Li Zhengping Niu Xiru Wu Jiangxi Xiao Yuwu Jiang Jingmin Wang

OBJECTIVE Hypomyelinating disorders are a group of clinically and genetically heterogeneous diseases characterized by neurological deterioration with hypomyelination visible on brain MRI scans. This study was aimed to clarify the clinical and genetic features of HMDs in Chinese population. METHODS 119 patients with hypomyelinating disorders in Chinese population were enrolled and evaluated ba...

2003
Mark P. Mattson Christine Van Broeckhoven John Hardy John Q. Trojanowski Alexander Gow Ramaswamy Sharma

For many genetic diseases, clinical phenotypes arise through the dysfunction of the gene products encoded by mutant genes. Effective treatment entails providing a source of the gene product in the diet or circulation, as has been achieved for type I diabetes and hemophilia, or in cases of enzyme deficiency by supplementation with metabolites synthesized by the defective protein, as in adrenoleu...

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