Editorial: Glial crosstalk in neurological disorders

Neurons have been focused as a main target for investigation of pathogenesis and therapeutics in neurological disorders. Although some of the mechanisms, including oxidative stress and inflammation, followed by apoptosis, are thought to be involved in the pathogenesis of these diseases, pathological...

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Detalles Bibliográficos
Autores: Miyazaki, Ikuko, Asanuma, Masato, Díaz-Corrales, Francisco J.
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2024
País:España
Institución:Consejo Superior de Investigaciones Científicas (CSIC)
Repositorio:DIGITAL.CSIC. Repositorio Institucional del CSIC
OAI Identifier:oai:digital.csic.es:10261/378217
Acceso en línea:http://hdl.handle.net/10261/378217
https://api.elsevier.com/content/abstract/scopus_id/85210165045
Access Level:acceso abierto
Palabra clave:Astrocyte
Glia
Glial interaction
Microglia
Neurological disorder
Oligodendrocyte
Descripción
Sumario:Neurons have been focused as a main target for investigation of pathogenesis and therapeutics in neurological disorders. Although some of the mechanisms, including oxidative stress and inflammation, followed by apoptosis, are thought to be involved in the pathogenesis of these diseases, pathological mechanism remains unknown. There is a consensus on the involvement of non-neuronal cells in the pathological progression. Recently, glial cells are getting attention as a key players of non-cell autonomous neurodegeneration in neurological disorders. Especially, glial crosstalk and its action on neurons are highlighted. It is demonstrated that microglia convert astrocytes to neurotoxic reactive A1 astrocytes (Liddelow, et al., 2017). In contrast, it is also reported that astrocytes activate microglia to produce neuroinflammation (Rohl and Sievers, 2005). Besides, astrocyte-microglia crosstalk contributes to degradation of protein aggregates (Rostami, et al., 2021). Furthermore, recent studies indicated microglia-oligodendrocyte or astrocyte-oligodendrocyte interaction promoted neuronal dysfunction and neurodegeneration (Lohrberg, et al., 2020; Papazian, et al., 2021). Thus, glial communication could be a main target to understand pathological mechanism and develop neuroprotective therapeutic approach. This series includes five articles covering different aspect of the Research Topic outlined above.