Synaptic pathology in multiple sclerosis: a role for Nogo-A signaling in astrocytes?

Espírito-Santo, Sheila; Coutinho, ViníciusGabriel; Gomes, FláviaCarvalho Alcantara

doi:10.4103/1673-5374.340407

Cited by 2 publications

(2 citation statements)

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“…Synaptopathy, as described in MS, occurs from an imbalance between formation/activity of excitatory (mainly glutamatergic) and inhibitory (GABAergic) synapses. As a result of such dysfunction, excitotoxicity ensues ( 44 ). Multiple studies have shown both in MS patients and in the EAE model that inflammatory infiltration of the CNS and cytokine release is directly correlated to synaptic loss in regions such as the hippocampus, the striatum and the neocortex.…”

Section: The Processes Behind Demyelinationmentioning

confidence: 99%

“…Nevertheless, what becomes undeniable is the impact of both glial and grey matter disease in MS. When looking into the clinical history of PPMS, some works (42,43) show that not only grey matter destruction is highly-prevalent, but it also occurs in somewhat related anatomical patterns, which, in turn, strongly correlate with clinical disabilities such as motor impairment and cognitive decline. Cognitive decline itself, while historically considered a secondary phenomenon in demyelinating diseases, has gained more attention recently.…”

Section: Myelin Destruction and Neurodegenerationmentioning

confidence: 99%

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Central nervous system demyelinating diseases: glial cells at the hub of pathology

et al. 2023

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Inflammatory demyelinating diseases (IDDs) are among the main causes of inflammatory and neurodegenerative injury of the central nervous system (CNS) in young adult patients. Of these, multiple sclerosis (MS) is the most frequent and studied, as it affects about a million people in the USA alone. The understanding of the mechanisms underlying their pathology has been advancing, although there are still no highly effective disease-modifying treatments for the progressive symptoms and disability in the late stages of disease. Among these mechanisms, the action of glial cells upon lesion and regeneration has become a prominent research topic, helped not only by the discovery of glia as targets of autoantibodies, but also by their role on CNS homeostasis and neuroinflammation. In the present article, we discuss the participation of glial cells in IDDs, as well as their association with demyelination and synaptic dysfunction throughout the course of the disease and in experimental models, with a focus on MS phenotypes. Further, we discuss the involvement of microglia and astrocytes in lesion formation and organization, remyelination, synaptic induction and pruning through different signaling pathways. We argue that evidence of the several glia-mediated mechanisms in the course of CNS demyelinating diseases supports glial cells as viable targets for therapy development.

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Section: The Processes Behind Demyelinationmentioning

confidence: 99%

Section: Myelin Destruction and Neurodegenerationmentioning

confidence: 99%