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Targeting senescence to delay progression of multiple sclerosis
Oost, W., Talma, N., Meilof, J. F. & Laman, J. D., Nov-2018, In : Journal of Molecular Medicine. 96, 11, p. 1153-1166 14 p.Research output: Contribution to journal › Review article › Academic › peer-review
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Targeting senescence to delay progression of multiple sclerosis. / Oost, Wendy; Talma, Nynke; Meilof, Jan F; Laman, Jon D.
In: Journal of Molecular Medicine, Vol. 96, No. 11, 11.2018, p. 1153-1166.Research output: Contribution to journal › Review article › Academic › peer-review
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TY - JOUR
T1 - Targeting senescence to delay progression of multiple sclerosis
AU - Oost, Wendy
AU - Talma, Nynke
AU - Meilof, Jan F
AU - Laman, Jon D
PY - 2018/11
Y1 - 2018/11
N2 - Multiple sclerosis (MS) is a chronic and often progressive, demyelinating disease of the central nervous system (CNS) white and gray matter and the single most common cause of disability in young adults. Age is one of the factors most strongly influencing the course of progression in MS. One of the hallmarks of aging is cellular senescence. The elimination of senescent cells with senolytics has very recently been shown to delay age-related dysfunction in animal models for other neurological diseases. In this review, the possible link between cellular senescence and the progression of MS is discussed, and the potential use of senolytics as a treatment for progressive MS is explored. Currently, there is no cure for MS and there are limited treatment options to slow the progression of MS. Current treatment is based on immunomodulatory approaches. Various cell types present in the CNS can become senescent and thus potentially contribute to MS disease progression. We propose that, after cellular senescence has indeed been shown to be directly implicated in disease progression, administration of senolytics should be tested as a potential therapeutic approach for the treatment of progressive MS.
AB - Multiple sclerosis (MS) is a chronic and often progressive, demyelinating disease of the central nervous system (CNS) white and gray matter and the single most common cause of disability in young adults. Age is one of the factors most strongly influencing the course of progression in MS. One of the hallmarks of aging is cellular senescence. The elimination of senescent cells with senolytics has very recently been shown to delay age-related dysfunction in animal models for other neurological diseases. In this review, the possible link between cellular senescence and the progression of MS is discussed, and the potential use of senolytics as a treatment for progressive MS is explored. Currently, there is no cure for MS and there are limited treatment options to slow the progression of MS. Current treatment is based on immunomodulatory approaches. Various cell types present in the CNS can become senescent and thus potentially contribute to MS disease progression. We propose that, after cellular senescence has indeed been shown to be directly implicated in disease progression, administration of senolytics should be tested as a potential therapeutic approach for the treatment of progressive MS.
KW - Aging
KW - Senolytics
KW - Glia
KW - Neurodegeneration
KW - Inflammation
KW - Autoimmunity
KW - CENTRAL-NERVOUS-SYSTEM
KW - VASCULAR ENDOTHELIAL-CELLS
KW - CD4(+)CD28(-) T-CELLS
KW - BLOOD-BRAIN-BARRIER
KW - CELLULAR SENESCENCE
KW - SECRETORY PHENOTYPE
KW - CNS REMYELINATION
KW - SENOLYTIC DRUGS
KW - PRECURSOR CELLS
KW - CANCER CELLS
U2 - 10.1007/s00109-018-1686-x
DO - 10.1007/s00109-018-1686-x
M3 - Review article
C2 - 30229272
VL - 96
SP - 1153
EP - 1166
JO - Journal of Molecular Medicine
JF - Journal of Molecular Medicine
SN - 0946-2716
IS - 11
ER -
ID: 65262611