Literature DB >> 12209119

Why does remyelination fail in multiple sclerosis?

Robin J M Franklin1.   

Abstract

Multiple sclerosis is a common cause of neurological disability in young adults. The disease is complex -- its aetiology is multifactorial and largely unknown; its pathology is heterogeneous; and, clinically, it is difficult to diagnose, manage and treat. However, perhaps its most frustrating aspect is the inadequacy of the healing response of remyelination. This regenerative process generally occurs with great efficiency in experimental models, and sometimes proceeds to completion in multiple sclerosis. But as the disease progresses, the numbers of lesions in which demyelination persists increases, significantly contributing to clinical deterioration. Understanding why remyelination fails is crucial for devising effective methods by which to enhance it.

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Year:  2002        PMID: 12209119     DOI: 10.1038/nrn917

Source DB:  PubMed          Journal:  Nat Rev Neurosci        ISSN: 1471-003X            Impact factor:   34.870


  277 in total

1.  Erk1/2 MAPK and mTOR signaling sequentially regulates progression through distinct stages of oligodendrocyte differentiation.

Authors:  Hebe M Guardiola-Diaz; Akihiro Ishii; Rashmi Bansal
Journal:  Glia       Date:  2011-12-05       Impact factor: 7.452

2.  Homocysteine and folate deficiency sensitize oligodendrocytes to the cell death-promoting effects of a presenilin-1 mutation and amyloid beta-peptide.

Authors:  Kirk J Pak; Sic L Chan; Mark P Mattson
Journal:  Neuromolecular Med       Date:  2003       Impact factor: 3.843

3.  Myelin repair is accelerated by inactivating CXCR2 on nonhematopoietic cells.

Authors:  LiPing Liu; Lindsey Darnall; Taofang Hu; Karen Choi; Thomas E Lane; Richard M Ransohoff
Journal:  J Neurosci       Date:  2010-07-07       Impact factor: 6.167

Review 4.  The potential of mesenchymal stromal cells as a novel cellular therapy for multiple sclerosis.

Authors:  Jeffery J Auletta; Amelia M Bartholomew; Richard T Maziarz; Robert J Deans; Robert H Miller; Hillard M Lazarus; Jeffrey A Cohen
Journal:  Immunotherapy       Date:  2012-05       Impact factor: 4.196

5.  Interferon-γ inhibits central nervous system myelination through both STAT1-dependent and STAT1-independent pathways.

Authors:  Wensheng Lin; Yifeng Lin
Journal:  J Neurosci Res       Date:  2010-09       Impact factor: 4.164

Review 6.  Oligodendrocyte regeneration: Its significance in myelin replacement and neuroprotection in multiple sclerosis.

Authors:  Kelly A Chamberlain; Sonia E Nanescu; Konstantina Psachoulia; Jeffrey K Huang
Journal:  Neuropharmacology       Date:  2015-10-22       Impact factor: 5.250

Review 7.  Gene expression changes underlying cortical pathology: clues to understanding neurological disability in multiple sclerosis.

Authors:  Ranjan Dutta
Journal:  Mult Scler       Date:  2013-09       Impact factor: 6.312

8.  Bone morphogenetic protein signaling and olig1/2 interact to regulate the differentiation and maturation of adult oligodendrocyte precursor cells.

Authors:  Xiaoxin Cheng; Yaping Wang; Qian He; Mengsheng Qiu; Scott R Whittemore; Qilin Cao
Journal:  Stem Cells       Date:  2007-09-13       Impact factor: 6.277

9.  Fibroblast growth factor signaling in oligodendrocyte-lineage cells facilitates recovery of chronically demyelinated lesions but is redundant in acute lesions.

Authors:  Miki Furusho; Aude J Roulois; Robin J M Franklin; Rashmi Bansal
Journal:  Glia       Date:  2015-04-22       Impact factor: 7.452

10.  g-Ratio weighted imaging of the human spinal cord in vivo.

Authors:  T Duval; S Le Vy; N Stikov; J Campbell; A Mezer; T Witzel; B Keil; V Smith; L L Wald; E Klawiter; J Cohen-Adad
Journal:  Neuroimage       Date:  2016-09-22       Impact factor: 6.556

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