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Probiotics ameliorate intestinal pathophysiology in a mouse model of Alzheimer's disease
Harpreet Kaur1, Kumi Nagamoto-Combs2, Svetlana Golovko1
1Department of Biomedical Sciences, University of North Dakota, School of Medicine & Health Sciences, Grand Forks, ND, USA.
Abstract:
Evidence suggests that changes in intestinal microbiota may affect the central nervous system. However, it is unclear whether alteration of intestinal microbiota affects progression of Alzheimer's disease (AD). To understand this, wild-type control (C57BL/6) mice were compared with the AppNL-G-F model of disease. We used probiotic supplementation to manipulate the gut microbiota. Fecal samples were collected for microbiota profiling. To study brain and intestinal inflammation, biochemical and histological analyses were performed. Altered metabolic pathways were examined by quantifying eicosanoid and bile acid profiles in the brain and serum using ultraperformance liquid chromatography-tandem mass spectrometry. We observed that brain pathology was associated with intestinal dysbiosis and increased intestinal inflammation and leakiness in AppNL-G-F mice. Probiotic supplementation significantly decreased intestinal inflammation and gut permeability with minimal effect on amyloid-β, cytokine, or gliosis levels in the brain. Concentrations of several bile acids and prostaglandins were altered in the serum and brain because of AD or probiotic supplementation. Our study characterizes intestinal dysfunction in an AD mouse model and the potential of probiotic intervention to ameliorate this condition.
Insights
Changes in gut bacteria are linked to Alzheimer's disease (AD) progression. Probiotic use reduced gut inflammation and leakiness in an AD mouse model, suggesting potential therapeutic benefits.
Area of Science:
- Neuroscience
- Microbiology
- Gastroenterology
Background:
- Emerging evidence links the gut microbiota to central nervous system function.
- The specific impact of intestinal microbiota alterations on Alzheimer's disease (AD) progression remains largely unknown.
Purpose of the Study:
- To investigate the relationship between intestinal microbiota, gut inflammation, and brain pathology in a mouse model of Alzheimer's disease.
- To evaluate the efficacy of probiotic supplementation in modulating the gut microbiota and mitigating AD-related pathology.
Main Methods:
- Comparison of wild-type mice with the AppNL-G-F Alzheimer's disease model.
- Manipulation of gut microbiota using probiotic supplementation.
- Analysis of fecal samples for microbiota profiling, and biochemical and histological analyses for brain and intestinal inflammation.
- Quantification of eicosanoid and bile acid profiles in brain and serum using ultraperformance liquid chromatography-tandem mass spectrometry.
Main Results:
- Alzheimer's disease model mice exhibited intestinal dysbiosis, increased intestinal inflammation, and gut leakiness.
- Probiotic supplementation significantly reduced intestinal inflammation and gut permeability.
- Probiotic intervention had minimal impact on amyloid-β, cytokine, or gliosis levels in the brain.
- Altered concentrations of specific bile acids and prostaglandins were observed in serum and brain due to AD and probiotic treatment.
Conclusions:
- Intestinal dysfunction is a feature of this Alzheimer's disease mouse model.
- Probiotic intervention shows potential for ameliorating intestinal dysfunction in Alzheimer's disease.
- Gut-brain axis modulation via probiotics warrants further investigation for Alzheimer's disease therapeutics.
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