Amantadine reduces sepsis-induced brain injury via NLRP3/caspase-1 inflammasome activation.

The pathophysiology of brain damage due to systemic inflammation is complex. Our findings suggest that amantadine reduces neuronal injury in the brain by alleviating oxidative stress and inflammation. Notably, amantadine's efficacy appears to extend beyond NMDA receptors, implicating involvement in alternative pathways, such as Cas-1 activation by the NLRP3 inflammasome.

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Publication Details

Journal
PubMed
Published
2025-01-01
DOI
https://doi.org/10.22038/ijbms.2025.81436.17626
Primary Topic
Intensive Care Unit Cognitive Disorders
Type
article
Field-Weighted Citation Impact
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article

Amantadine reduces sepsis-induced brain injury via NLRP3/caspase-1 inflammasome activation.

Muhammet Yusuf Tepebaşı, Mustafa Soner Özcan, Halil Aşçı, Pınar Karabacak et al.
PubMed
Intensive Care Unit Cognitive Disorders
article

Amantadine reduces sepsis-induced brain injury via NLRP3/caspase-1 inflammasome activation.

Muhammet Yusuf Tepebaşı, Mustafa Soner Özcan, Halil Aşçı, Pınar Karabacak, Rümeysa Taner, İlter İlhan, Melih Arlıoğlu, Ahmet Bi̇ndal
article en

Abstract

The pathophysiology of brain damage due to systemic inflammation is complex. Our findings suggest that amantadine reduces neuronal injury in the brain by alleviating oxidative stress and inflammation. Notably, amantadine's efficacy appears to extend beyond NMDA receptors, implicating involvement in alternative pathways, such as Cas-1 activation by the NLRP3 inflammasome.

PubMedVol. 28(5)
Süleyman Demirel Üniversitesi (TR), Suleyman Demirel University (KZ)
Openalex Percentile: Top 79%
Intensive Care Unit Cognitive Disorders
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