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Microglia and status epilepticus in the immature brain

Microglia are the resident immune cells of the Central Nervous System (CNS), which are activated due to brain damage, as part of the neuroinflammatory response. Microglia undergo morphological and biochemical modifications during activation, adopting a pro‐inflammatory or an antiinflammatory state....

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Detalles Bibliográficos
Autores principales: López‐Meraz, Maria‐Leonor, Álvarez‐Croda, Dulce‐Mariely
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173848/
https://www.ncbi.nlm.nih.gov/pubmed/35531942
http://dx.doi.org/10.1002/epi4.12610
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author López‐Meraz, Maria‐Leonor
Álvarez‐Croda, Dulce‐Mariely
author_facet López‐Meraz, Maria‐Leonor
Álvarez‐Croda, Dulce‐Mariely
author_sort López‐Meraz, Maria‐Leonor
collection PubMed
description Microglia are the resident immune cells of the Central Nervous System (CNS), which are activated due to brain damage, as part of the neuroinflammatory response. Microglia undergo morphological and biochemical modifications during activation, adopting a pro‐inflammatory or an antiinflammatory state. In the developing brain, status epilepticus (SE) promotes microglia activation that is associated with neuronal injury in some areas of the brain, such as the hippocampus, thalamus, and amygdala. However, the timing of this activation, the anatomical pattern, and the morphological and biochemical characteristics of microglia in the immature brain are age‐dependent and have not been fully characterized. Therefore, this review focuses on the response of microglia to SE and its relationship to neurodegeneration.
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spelling pubmed-101738482023-05-12 Microglia and status epilepticus in the immature brain López‐Meraz, Maria‐Leonor Álvarez‐Croda, Dulce‐Mariely Epilepsia Open Critical Review–Invited Commentary Microglia are the resident immune cells of the Central Nervous System (CNS), which are activated due to brain damage, as part of the neuroinflammatory response. Microglia undergo morphological and biochemical modifications during activation, adopting a pro‐inflammatory or an antiinflammatory state. In the developing brain, status epilepticus (SE) promotes microglia activation that is associated with neuronal injury in some areas of the brain, such as the hippocampus, thalamus, and amygdala. However, the timing of this activation, the anatomical pattern, and the morphological and biochemical characteristics of microglia in the immature brain are age‐dependent and have not been fully characterized. Therefore, this review focuses on the response of microglia to SE and its relationship to neurodegeneration. John Wiley and Sons Inc. 2022-05-17 /pmc/articles/PMC10173848/ /pubmed/35531942 http://dx.doi.org/10.1002/epi4.12610 Text en © 2022 The Authors. Epilepsia Open published by Wiley Periodicals LLC on behalf of International League Against Epilepsy. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Critical Review–Invited Commentary
López‐Meraz, Maria‐Leonor
Álvarez‐Croda, Dulce‐Mariely
Microglia and status epilepticus in the immature brain
title Microglia and status epilepticus in the immature brain
title_full Microglia and status epilepticus in the immature brain
title_fullStr Microglia and status epilepticus in the immature brain
title_full_unstemmed Microglia and status epilepticus in the immature brain
title_short Microglia and status epilepticus in the immature brain
title_sort microglia and status epilepticus in the immature brain
topic Critical Review–Invited Commentary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173848/
https://www.ncbi.nlm.nih.gov/pubmed/35531942
http://dx.doi.org/10.1002/epi4.12610
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