Astrocytes in the initiation and progression of epilepsy.


Journal

Nature reviews. Neurology
ISSN: 1759-4766
Titre abrégé: Nat Rev Neurol
Pays: England
ID NLM: 101500072

Informations de publication

Date de publication:
12 2022
Historique:
accepted: 16 09 2022
pubmed: 26 10 2022
medline: 1 12 2022
entrez: 25 10 2022
Statut: ppublish

Résumé

Epilepsy affects ~65 million people worldwide. First-line treatment options include >20 antiseizure medications, but seizure control is not achieved in approximately one-third of patients. Antiseizure medications act primarily on neurons and can provide symptomatic control of seizures, but do not alter the onset and progression of epilepsy and can cause serious adverse effects. Therefore, medications with new cellular and molecular targets and mechanisms of action are needed. Accumulating evidence indicates that astrocytes are crucial to the pathophysiological mechanisms of epilepsy, raising the possibility that these cells could be novel therapeutic targets. In this Review, we discuss how dysregulation of key astrocyte functions - gliotransmission, cell metabolism and immune function - contribute to the development and progression of hyperexcitability in epilepsy. We consider strategies to mitigate astrocyte dysfunction in each of these areas, and provide an overview of how astrocyte activation states can be monitored in vivo not only to assess their contribution to disease but also to identify markers of disease processes and treatment effects. Improved understanding of the roles of astrocytes in epilepsy has the potential to lead to novel therapies to prevent the initiation and progression of epilepsy.

Identifiants

pubmed: 36280704
doi: 10.1038/s41582-022-00727-5
pii: 10.1038/s41582-022-00727-5
pmc: PMC10368155
mid: NIHMS1914868
doi:

Types de publication

Journal Article Review Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

707-722

Subventions

Organisme : NINDS NIH HHS
ID : R01 NS103740
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS061844
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS065957
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS127846
Pays : United States

Informations de copyright

© 2022. Springer Nature Limited.

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Auteurs

Annamaria Vezzani (A)

Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milano, Italy. annamaria.vezzani@marionegri.it.

Teresa Ravizza (T)

Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milano, Italy.

Peter Bedner (P)

Institute of Cellular Neurosciences, Medical Faculty, University of Bonn, Bonn, Germany.

Eleonora Aronica (E)

Amsterdam UMC, University of Amsterdam, Department of (Neuro)Pathology, Amsterdam Neuroscience, Amsterdam, Netherlands.
Stichting Epilepsie Instellingen Nederland (SEIN), Heemstede, Netherlands.

Christian Steinhäuser (C)

Institute of Cellular Neurosciences, Medical Faculty, University of Bonn, Bonn, Germany.

Detlev Boison (D)

Department of Neurosurgery, Robert Wood Johnson Medical School, Rutgers University, Piscataway, NJ, USA.

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Classifications MeSH