Gut microbiome alterations in Alzheimer's disease

Gut microbiome alterations in Alzheimer's disease

19 October 2017 | Nicholas M. Vogt, Robert L. Kerby, Kimberly A. Dill-McFarland, Sandra J. Harding, Andrew P. Merluzzi, Sterling C. Johnson, Cynthia M. Carlsson, Sanjay Asthana, Henrik Zetterberg, Kaj Blennow, Barbara B. Bendlin, Federico E. Rey
Alzheimer's disease (AD) is a common form of dementia with unknown etiology. Recent studies suggest that gut microbiome alterations may contribute to AD pathology. This study characterized the gut microbiome of individuals with and without AD, revealing decreased microbial diversity and distinct composition in AD participants. Phylum- and genus-level differences were observed, including reduced Firmicutes and Bifidobacterium, and increased Bacteroidetes. Correlations between microbial abundance and CSF biomarkers of AD pathology were identified. These findings suggest that gut microbial communities may be a therapeutic target for AD. The gut microbiome is complex, with most microbes residing in the gut, and its composition is stable after early childhood. Alterations in the gut microbiome have been linked to various diseases, including neurological conditions. In AD, gut microbiota may influence amyloid deposition and neuroinflammation. The study found that AD participants had altered gut microbiota, with increased Bacteroidetes and decreased Actinobacteria. Functional analysis showed changes in predicted metabolism and signaling pathways. Correlations between microbial abundance and AD biomarkers were observed, with certain genera associated with greater AD pathology. These findings highlight the potential role of gut microbiota in AD pathogenesis and suggest that targeting gut bacteria may offer therapeutic approaches. Further research is needed to explore the relationship between gut microbiota and AD.Alzheimer's disease (AD) is a common form of dementia with unknown etiology. Recent studies suggest that gut microbiome alterations may contribute to AD pathology. This study characterized the gut microbiome of individuals with and without AD, revealing decreased microbial diversity and distinct composition in AD participants. Phylum- and genus-level differences were observed, including reduced Firmicutes and Bifidobacterium, and increased Bacteroidetes. Correlations between microbial abundance and CSF biomarkers of AD pathology were identified. These findings suggest that gut microbial communities may be a therapeutic target for AD. The gut microbiome is complex, with most microbes residing in the gut, and its composition is stable after early childhood. Alterations in the gut microbiome have been linked to various diseases, including neurological conditions. In AD, gut microbiota may influence amyloid deposition and neuroinflammation. The study found that AD participants had altered gut microbiota, with increased Bacteroidetes and decreased Actinobacteria. Functional analysis showed changes in predicted metabolism and signaling pathways. Correlations between microbial abundance and AD biomarkers were observed, with certain genera associated with greater AD pathology. These findings highlight the potential role of gut microbiota in AD pathogenesis and suggest that targeting gut bacteria may offer therapeutic approaches. Further research is needed to explore the relationship between gut microbiota and AD.
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