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Differences in gut microbiota composition between ischemic stroke patients and healthy individuals.

Created on 30 Jun 2026

Authors

Mohammadreza Movahedi, Somayeh Ahmadi, Sama Rahnemayan, Kaveh Mehrvar

Published in

BMC neurology. Jun 29, 2026. Epub Jun 29, 2026.

Abstract

Ischemic stroke is a leading cause of mortality and disability worldwide. Emerging evidence suggests that the gut microbiota, acting through the gut-brain axis, may play a critical role in stroke pathophysiology. Dysbiosis, an imbalance of gut microbiota, has been associated with neuroinflammation and poor stroke outcomes. This study aimed to compare gut microbiota composition in ischemic stroke patients versus healthy controls to explore potential microbial changes linked to stroke.
A case-control study was conducted on 30 ischemic stroke patients and 30 healthy age- and gender-matched controls. Fecal samples were analyzed using real-time PCR to assess the relative abundance of four key gut bacterial phyla (Firmicutes, Bacteroidetes, Proteobacteria, Actinobacteria). Statistical analysis was performed with SPSS, and results were considered significant at p < 0.05.
Ischemic stroke patients exhibited significant alterations in gut microbiota composition compared to controls. Firmicutes levels were significantly decreased (p = 0.04), while Proteobacteria levels were significantly elevated (p = 0.003). Although reductions in Bacteroidetes and Actinobacteria were observed, these differences were not statistically significant. The Firmicutes-to-Bacteroidetes (F/B) ratio was increased in ischemic stroke patients, indicating dysbiosis associated with stroke.
The study identified gut microbiota dysbiosis in ischemic stroke patients, suggesting its potential role in stroke pathophysiology. Reduced Firmicutes and increased Proteobacteria may contribute to inflammation and oxidative stress, potentially worsening stroke outcomes. These findings highlight the potential for gut microbiota modulation as a therapeutic strategy to improve stroke management and recovery.

PMID:
42374255
Bibliographic data and abstract were imported from PubMed on 30 Jun 2026.

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