Osorio M Joana, Rowitch David H, Tesar Paul, Wernig Marius, Windrem Martha S, Goldman Steven A
Center for Basic and Translational Neuroscience, University of Copenhagen, Copenhagen, Denmark.
Departments of Pediatrics and Neurosurgery, UCSF School of Medicine and Broad Center for Regenerative Medicine, San Francisco, California, USA.
Stem Cells. 2017 Feb;35(2):311-315. doi: 10.1002/stem.2530. Epub 2016 Nov 23.
Pelizaeus-Merzbacher disease (PMD) is an X-linked disorder caused by mutation in the proteolipid protein-1 (PLP1) gene, which encodes the proteolipid protein of myelinating oligodendroglia. PMD exhibits phenotypic variability that reflects its considerable genotypic heterogeneity, but all forms of the disease result in central hypomyelination, associated in most cases with early neurological dysfunction, progressive deterioration, and ultimately death. PMD may present as a connatal, classic and transitional forms, or as the less severe spastic paraplegia type 2 and PLP-null phenotypes. These disorders are most often associated with duplications of the PLP1 gene, but can also be caused by coding and noncoding point mutations as well as full or partial deletion of the gene. A number of genetically-distinct but phenotypically-similar disorders of hypomyelination exist which, like PMD, lack any effective therapy. Yet as relatively pure CNS hypomyelinating disorders, with limited involvement of the PNS and relatively little attendant neuronal pathology, PMD and similar hypomyelinating disorders are attractive therapeutic targets for neural stem cell and glial progenitor cell transplantation, efforts at which are now underway in a number of research centers. Stem Cells 2017;35:311-315.
佩利措伊斯-梅茨巴赫病(PMD)是一种X连锁疾病,由蛋白脂蛋白-1(PLP1)基因突变引起,该基因编码髓鞘少突胶质细胞的蛋白脂蛋白。PMD表现出表型变异性,反映了其显著的基因型异质性,但所有形式的疾病都会导致中枢性髓鞘形成不足,在大多数情况下与早期神经功能障碍、进行性恶化以及最终死亡相关。PMD可能表现为先天性、经典型和过渡型,或表现为较轻的痉挛性截瘫2型和PLP基因缺失表型。这些疾病最常与PLP1基因重复相关,但也可能由编码和非编码点突变以及该基因的全部或部分缺失引起。存在一些基因上不同但表型相似的髓鞘形成不足疾病,与PMD一样,缺乏任何有效治疗方法。然而,作为相对纯粹的中枢神经系统髓鞘形成不足疾病,周围神经系统受累有限且伴随的神经元病理学相对较少,PMD和类似的髓鞘形成不足疾病是神经干细胞和神经胶质祖细胞移植有吸引力的治疗靶点,目前许多研究中心正在进行这方面的努力。《干细胞》2017年;35卷:311 - 315页