TY - JOUR
T1 - Chronic oligodendrocyte injury in central nervous system pathologies
AU - Molina-Gonzalez, Irene
AU - Miron, Véronique E
AU - Antel, Jack P.
N1 - Funding Information:
I.M.-G. and V.E.M. are supported by a Medical Research Council Senior Non-Clinical Fellowship (to V.E.M.) and the United Kingdom Dementia Research Institute at The University of Edinburgh in partnership with Astex Pharmaceuticals. V.E.M. is supported by the John David Eaton Chair in Multiple Sclerosis Research at the Barlo Multiple Sclerosis Centre. J.A. received support from the Progressive MS Alliance MSIF. We thank Tanja Kuhlmann for critical feedback. Diagrams were created using BioRender.com.
Publisher Copyright:
© 2022, The Author(s).
PY - 2022/11/19
Y1 - 2022/11/19
N2 - Myelin, the membrane surrounding neuronal axons, is critical for central nervous system (CNS) function. Injury to myelin-forming oligodendrocytes (OL) in chronic neurological diseases (e.g. multiple sclerosis) ranges from sublethal to lethal, leading to OL dysfunction and myelin pathology, and consequent deleterious impacts on axonal health that drive clinical impairments. This is regulated by intrinsic factors such as heterogeneity and age, and extrinsic cellular and molecular interactions. Here, we discuss the responses of OLs to injury, and perspectives for therapeutic targeting. We put forward that targeting mature OL health in neurological disease is a promising therapeutic strategy to support CNS function.
AB - Myelin, the membrane surrounding neuronal axons, is critical for central nervous system (CNS) function. Injury to myelin-forming oligodendrocytes (OL) in chronic neurological diseases (e.g. multiple sclerosis) ranges from sublethal to lethal, leading to OL dysfunction and myelin pathology, and consequent deleterious impacts on axonal health that drive clinical impairments. This is regulated by intrinsic factors such as heterogeneity and age, and extrinsic cellular and molecular interactions. Here, we discuss the responses of OLs to injury, and perspectives for therapeutic targeting. We put forward that targeting mature OL health in neurological disease is a promising therapeutic strategy to support CNS function.
U2 - 10.1038/s42003-022-04248-1
DO - 10.1038/s42003-022-04248-1
M3 - Article
VL - 5
JO - Communications biology
JF - Communications biology
SN - 2399-3642
M1 - 1274
ER -