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1 is the most common molecular abnormality in Pelizaeus Merzbacher disease.
2 ertain human demyelinating diseases, such as Pelizaeus-Merzbacher disease.
3 y linked to another myelin-related disorder, Pelizaeus-Merzbacher disease.
4 Finally, iOPCs derived from patients with Pelizaeus Merzbacher disease, a hypomyelinating leukodys
5 of misfolded proteins in the leukodystrophy Pelizaeus-Merzbacher disease activates this stress respo
6 oteolipid protein gene is the major cause of Pelizaeus-Merzbacher disease, an X-linked central nervou
7 g with severe leukodystrophy compatible with Pelizaeus-Merzbacher disease and peripheral neuropathy c
8 elin, including Charcot-Marie-Tooth disease, Pelizaeus-Merzbacher disease and Vanishing White Matter
10 rolled expression of Plp1, as illustrated by Pelizaeus-Merzbacher disease for which the most common c
14 The shaking (sh) pup, an animal model of Pelizaeus-Merzbacher disease, is characterized by severe
16 ical to the initiation of myelination, as in Pelizaeus-Merzbacher Disease, or to enzymatic deficienci
17 nstrate UPR activation in the leukodystrophy Pelizaeus-Merzbacher disease (PMD) as well as in three m
31 continuum of phenotypes ranging from severe Pelizaeus-Merzbacher disease (PMD) to uncomplicated HSP
32 t families with an atypically severe form of Pelizaeus-Merzbacher disease (PMD) who have three, and i
35 In man, mutations of these proteins cause Pelizaeus-Merzbacher disease (PMD), an X-linked dysmyeli
36 astic paraplegia type 2 (SPG2) is allelic to Pelizaeus-Merzbacher disease (PMD), with both conditions
40 plication mutation, the most common cause of Pelizaeus-Merzbacher disease, the pathology is poorly de
41 e embryonic myelin-deficient rat, a model of Pelizaeus-Merzbacher disease, was performed to assess th
42 The initial clinical presentation resembled Pelizaeus-Merzbacher disease with congenital nystagmus,