| Literature DB >> 26618372 |
Markus Kipp1,2.
Abstract
Remyelination is the natural repair mechanism of demyelination and can be a highly efficient process in multiple sclerosis. However, in the majority of lesions, this regenerative approach is incomplete or fails. It is believed that remyelination protects against progressive axonal damage and thus long-term disability in patients with multiple sclerosis. For this reason, therapeutic promotion of remyelination represents an attractive option for preventing disease progression. In this editorial we casts a critical eye over the most frequently used experimental settings which aim to uncover potential remyelination promoting drugs. This article reflects upon the personal opinion of the author who currently used animal models allow to assess the potency of pharmacological interventions to accelerate, but not to induce myelin repair. Furthermore, it is discussed how remyelination and neuroprotection might well be two separate entities. Thus, induction of remyelination does not necessarily prevent disease progression in multiple sclerosis patients.Entities:
Keywords: anima models; axonal damage; multiple sclerosis; neuroprotection; oligodendrocytes; remyelination
Mesh:
Year: 2015 PMID: 26618372 DOI: 10.1586/14737175.2016.1116387
Source DB: PubMed Journal: Expert Rev Neurother ISSN: 1473-7175 Impact factor: 4.618