Gut microbiome alterations in Alzheimer’s disease

Alzheimer’s disease (AD) is the most common form of dementia. However, the etiopathogenesis of this devastating disease is not fully understood. Recent studies in rodents suggest that alterations in the gut microbiome may contribute to amyloid deposition, yet the microbial communities associated wit...

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Published inScientific reports Vol. 7; no. 1; pp. 13537 - 11
Main Authors Vogt, Nicholas M., Kerby, Robert L., Dill-McFarland, Kimberly A., Harding, Sandra J., Merluzzi, Andrew P., Johnson, Sterling C., Carlsson, Cynthia M., Asthana, Sanjay, Zetterberg, Henrik, Blennow, Kaj, Bendlin, Barbara B., Rey, Federico E.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 19.10.2017
Nature Publishing Group
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Summary:Alzheimer’s disease (AD) is the most common form of dementia. However, the etiopathogenesis of this devastating disease is not fully understood. Recent studies in rodents suggest that alterations in the gut microbiome may contribute to amyloid deposition, yet the microbial communities associated with AD have not been characterized in humans. Towards this end, we characterized the bacterial taxonomic composition of fecal samples from participants with and without a diagnosis of dementia due to AD. Our analyses revealed that the gut microbiome of AD participants has decreased microbial diversity and is compositionally distinct from control age- and sex-matched individuals. We identified phylum- through genus-wide differences in bacterial abundance including decreased Firmicutes, increased Bacteroidetes, and decreased Bifidobacterium in the microbiome of AD participants. Furthermore, we observed correlations between levels of differentially abundant genera and cerebrospinal fluid (CSF) biomarkers of AD. These findings add AD to the growing list of diseases associated with gut microbial alterations, as well as suggest that gut bacterial communities may be a target for therapeutic intervention.
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ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-017-13601-y