Abstract
Neuroinflammation in cortical and meningeal pathology in multiple sclerosis: understanding from animal models
Highlights
Multiple sclerosis (MS) is a neurodegenerative and inflammatory disease of unknown etiology characterized by repeated inflammatory events, demyelination and axonal damage which cause loss of function in the central nervous system (CNS)[1]
MS displays different clinical patterns: recurrent episodes with periods of remission classified as relapsing-remitting MS (RRMS), which can progress to secondary progressive form (SPMS), or persistent progression from the onset of the disease classified as primary progressive MS (PPMS) [2]
Two theories tried to explain the relationship between cortical damage and meningeal inflammation; it was suggested that meningeal inflammation may play a role in the pathogenesis of cortical pathology (“outside-in” theory), but it is plausible that cortical damage could induce meningeal inflammation (“inside-out” theory)[8]
Summary
Multiple sclerosis (MS) is a neurodegenerative and inflammatory disease of unknown etiology characterized by repeated inflammatory events, demyelination and axonal damage which cause loss of function in the central nervous system (CNS)[1]. It has been previously demonstrated that immune cell infiltration and inflammation within the meninges correlate with the degree of GM demyelination, microglial activation, axonal pathology, and neuronal loss[14,15,16]. The ideal preclinical animal model that represents the cortical damage of progressive MS should include GM pathology with chronic demyelination, neurodegeneration, neuroinflammation with innate and adaptive immune infiltrate, and glial activation[18,19].
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