The NLRP3 Inflammasome in Neurodegenerative Disorders: Insights from Epileptic Models.
NLRP3 inflammasome
epilepsy
epileptogenesis
glutammate
kainic acid
neurodegeneration
neuroinflammation
pilocarpine
Journal
Biomedicines
ISSN: 2227-9059
Titre abrégé: Biomedicines
Pays: Switzerland
ID NLM: 101691304
Informations de publication
Date de publication:
18 Oct 2023
18 Oct 2023
Historique:
received:
20
09
2023
revised:
12
10
2023
accepted:
16
10
2023
medline:
28
10
2023
pubmed:
28
10
2023
entrez:
28
10
2023
Statut:
epublish
Résumé
Neuroinflammation represents a dynamic process of defense and protection against the harmful action of infectious agents or other detrimental stimuli in the central nervous system (CNS). However, the uncontrolled regulation of this physiological process is strongly associated with serious dysfunctional neuronal issues linked to the progression of CNS disorders. Moreover, it has been widely demonstrated that neuroinflammation is linked to epilepsy, one of the most prevalent and serious brain disorders worldwide. Indeed, NLRP3, one of the most well-studied inflammasomes, is involved in the generation of epileptic seizures, events that characterize this pathological condition. In this context, several pieces of evidence have shown that the NLRP3 inflammasome plays a central role in the pathophysiology of mesial temporal lobe epilepsy (mTLE). Based on an extensive review of the literature on the role of NLRP3-dependent inflammation in epilepsy, in this review we discuss our current understanding of the connection between NLRP3 inflammasome activation and progressive neurodegeneration in epilepsy. The goal of the review is to cover as many of the various known epilepsy models as possible, providing a broad overview of the current literature. Lastly, we also propose some of the present therapeutic strategies targeting NLRP3, aiming to provide potential insights for future studies.
Identifiants
pubmed: 37893198
pii: biomedicines11102825
doi: 10.3390/biomedicines11102825
pmc: PMC10604217
pii:
doi:
Types de publication
Journal Article
Review
Langues
eng
Subventions
Organisme : European Research Council
ID : 853057-InflaPML
Pays : International
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