Abstract:
:Multiple sclerosis (MS) is a chronic autoimmune inflammatory disease of the central nervous system (CNS) affecting more than 2.5 million individuals worldwide. In the present study, myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) mice were treated with adenosine receptor A2A antagonist SCH58261 at different periods of EAE development. The administration of SCH58261 at 11-28 days post-immunization (d.p.i.) with MOG improved the neurological deficits. This time window corresponds to the therapeutic time window for MS treatment. SCH58261 significantly reduced the CNS neuroinflammation including reduced local infiltration of inflammatory cells, demyelination, and the numbers of macrophage/microglia in the spinal cord. Importantly, SCH58261 ameliorated the EAE-induced neurobehavioral deficits. By contrast, the SCH58261 treatment was ineffective when administered at the beginning of the onset of EAE (i.e., 1-10 d.p.i). The identification of the effective therapeutic window of A2A receptor antagonist provide insight into the role of A2A receptor signaling in EAE, and support SCH58261 as a candidate for the treatment of MS in human.
journal_name
Neurochem Intjournal_title
Neurochemistry internationalauthors
Chen Y,Zhang ZX,Zheng LP,Wang L,Liu YF,Yin WY,Chen YY,Wang XS,Hou ST,Chen JF,Zheng RYdoi
10.1016/j.neuint.2019.104490subject
Has Abstractpub_date
2019-10-01 00:00:00pages
104490eissn
0197-0186issn
1872-9754pii
S0197-0186(19)30135-4journal_volume
129pub_type
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