Journal
MECHANISMS OF AGEING AND DEVELOPMENT
Volume 192, Issue -, Pages -Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mad.2020.111366
Keywords
Cellular senescence; Remyelination; Multiple sclerosis; Oligodendrocyte progenitor; Oligodendrocyte
Categories
Funding
- National Public Investment Program of the Ministry of Development and Investment/General Secretariat for Research and Technology [2020SigmaE01300001]
- European Union's Horizon 2020 research and innovation program under the Marie Sklodowska-Curie grant [722729]
- Welfare Foundation for Social & Cultural Sciences (KIKPE), Greece
- Pentagon Biotechnology, UK
- Hellenic Foundation for Research Innovation [775]
- NKUA-SARG [70/3/9816, 70/3/12128]
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Remyelination is a physiological response to demyelinating events aiming to restore saltatory conduction and preserve axonal integrity. Resident oligodendrocyte precursor cells (OPC) of the CNS tissue under appropriate conditions are mobilized to proliferate, migrate, and differentiate, in order to produce new myelin sheaths in the demyelinated lesion. In multiple sclerosis (MS), the most common immune-mediated demyelinating disease, remyelination efficiency declines with increasing age and disease duration. As myelin regeneration attempts in clinical trials so far are scarce, and have been met with limited success, the need to explore new remyelinating strategies is more compelling. Recently, ageing and cellular senescence have been implicated in the pathophysiology of a number of neurodegenerative diseases, including multiple sclerosis. Evidence on OPC senescence brings forward the possibility of exploiting cellular senescence as a possible target for promoting the endogenous remyelinating capacity of the CNS. Here we discuss the data indicating how cellular senescence affects remyelination, and the putative benefits to be drawn through the use of senolytic or senomorphic therapies targeting senescent cell populations in MS.
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