نتایج جستجو برای: remyelination

تعداد نتایج: 1550  

2016
Feng Mei Klaus Lehmann-Horn Yun-An A Shen Kelsey A Rankin Karin J Stebbins Daniel S Lorrain Kara Pekarek Sharon A Sagan Lan Xiao Cory Teuscher H-Christian von Büdingen Jürgen Wess J Josh Lawrence Ari J Green Stephen Pj Fancy Scott S Zamvil Jonah R Chan

Demyelination in MS disrupts nerve signals and contributes to axon degeneration. While remyelination promises to restore lost function, it remains unclear whether remyelination will prevent axonal loss. Inflammatory demyelination is accompanied by significant neuronal loss in the experimental autoimmune encephalomyelitis (EAE) mouse model and evidence for remyelination in this model is complica...

2015

Remyelination in the CNS: from biology to therapy. This finding confirms that remyelination must be a major therapeutic target in MS and the inherited human myelin disorders. 2008 Remyelination in the CNS: From biology to therapy. Masthead PDFIn stark contrast to the situation that follows loss of neurons or axonal damage, remyelination in the CNS can be a highly effective regenerative process....

Journal: :Brain : a journal of neurology 2013
Josephine M J Stoffels Jenny C de Jonge Mirjana Stancic Anita Nomden Miriam E van Strien Dan Ma Zuzana Sisková Olaf Maier Charles Ffrench-Constant Robin J M Franklin Dick Hoekstra Chao Zhao Wia Baron

Remyelination following central nervous system demyelination is essential to prevent axon degeneration. However, remyelination ultimately fails in demyelinating diseases such as multiple sclerosis. This failure of remyelination is likely mediated by many factors, including changes in the extracellular signalling environment. Here, we examined the expression of the extracellular matrix molecule ...

Journal: :Journal of Neuroimmunology 2015
Maria Nordheim Alme Agnes E. Nystad Lars Bø Kjell-Morten Myhr Christian A. Vedeler Stig Wergeland Øivind Torkildsen

Fingolimod (FTY720) is approved for treatment of relapsing-remitting multiple sclerosis. In vitro studies have found that fingolimod stimulates remyelination in cerebellar slices, but in vivo animal studies have not detected any positive effect on cerebral remyelination. The discrepant findings could be a result of different mechanisms underlying cerebral and cerebellar remyelination. The cupri...

2014
Hilary H. Sachs Kathryn K. Bercury Daniela C. Popescu S. Priya Narayanan Wendy B. Macklin

In the central nervous system, demyelinating diseases, such as multiple sclerosis, result in devastating long-term neurologic damage, in part because of the lack of effective remyelination in the adult human brain. One model used to understand the mechanisms regulating remyelination is cuprizone-induced demyelination, which allows investigation of remyelination mechanisms in adult animals follo...

Journal: :The American journal of pathology 2015
Glaucia Monteiro de Castro Natalia A Deja Dan Ma Chao Zhao Robin J M Franklin

Remyelination within the central nervous system (CNS) most often is the result of oligodendrocyte progenitor cells differentiating into myelin-forming oligodendrocytes. In some cases, however, Schwann cells, the peripheral nervous system myelinating glia, are found remyelinating demyelinated regions of the CNS. The reason for this peripheral type of remyelination in the CNS and what governs it ...

Journal: :Journal of neurology, neurosurgery, and psychiatry 1994
B G van Engelen D J Miller K D Pavelko O R Hommes M Rodriguez

Spontaneous remyelination occurs in experimental models of demyelination and in patients with multiple sclerosis, although to a limited extent. This enables the search for factors that promote remyelination. Using the Theiler's virus model of central nervous system demyelination, promotion of remyelination was observed after passive transfer of CNS-specific antiserum and transfer of CNS-specifi...

2015
Danielle E. Harlow Justin M. Honce Augusto A. Miravalle

Multiple sclerosis (MS) is an immune-mediated disorder of the central nervous system that results in destruction of the myelin sheath that surrounds axons and eventual neurodegeneration. Current treatments approved for the treatment of relapsing forms of MS target the aberrant immune response and successfully reduce the severity of attacks and frequency of relapses. Therapies are still needed t...

2014
Eva Jolanda Münzel Catherina G Becker Thomas Becker Anna Williams

INTRODUCTION In the human demyelinating central nervous system (CNS) disease multiple sclerosis, remyelination promotes recovery and limits neurodegeneration, but this is inefficient and always ultimately fails. Furthermore, these regenerated myelin sheaths are thinner and shorter than the original, leaving the underlying axons potentially vulnerable. In rodent models, CNS remyelination is more...

Journal: :Glia 2013
Sabine Pfeifenbring Imke Metz David Kremer Patrick Küry Hans-Peter Hartung Wolfgang Brück

Impaired remyelination in multiple sclerosis (MS) might be due to the failure of oligodendrocyte precursor cells (OPC) to differentiate into myelinating oligodendrocytes. Animal experimental data have shown that p57kip2 inhibits oligodendroglial differentiation, indicating that this factor could contribute to remyelination failure. This study investigates oligodendroglial p57kip2 expression and...

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