Abstract
Ischemic stroke (IS) and multiple sclerosis (MS) are two pathologies of the central nervous system (CNS). At the first look, this appears to be the only similarity between the two diseases, as they seem quite different. Indeed IS has an acute onset compared to MS which develops chronically; IS is consecutive to blood clot migrating to cerebral blood vessels or decrease in cerebral blood flow following atherosclerosis or decreases in cardiac output, whereas MS is an immune disease associated with neurodegeneration. However, both pathologies share similar pathologic pathways and treatments used in MS have been the object of studies in IS. In this mini-review we will discuss similarities between IS and MS on astrocytes and neuroinflammation hallmarks emphasizing the potential for treatments.
Highlights
Ischemic stroke (IS) and multiple sclerosis (MS) are two pathologies of the central nervous system (CNS)
It has been proposed that the two pathologies may share similar pathological pathways involving glutamate release, oxidative stress, and reactive oxygen species (ROS)
Results were discouraging as patients treated with lenercept suffered from increased disease activity. These results suggest that non-selective blockade of TNF-α is detrimental
Summary
Ischemic stroke (IS) and multiple sclerosis (MS) are two pathologies of the central nervous system (CNS). It has been proposed that the two pathologies may share similar pathological pathways involving glutamate release, oxidative stress, and reactive oxygen species (ROS). During IS, activation of glutamate receptors following the release of this excitatory neurotransmitter leads to an increase in intracellular calcium and activation of nitric oxide synthase and NADPH oxidase pathways. The resulting increases in ROS contribute to neuronal death, increases in blood–brain barrier (BBB) permeability and ischemic lesion development (for review see Forrester et al, 2018). Oligodendrocytes, the myelin-producing cells of the CNS, are vulnerable to glutamate excitotoxicity via glutamate receptors activation. ROS generated following glutamate receptors activation may contribute to demyelination and neuronal degradation in MS (for review, see Gilgun-Sherki et al, 2004; Iodice et al, 2017)
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