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Sci Rep. 2017 Oct 19;7(1):13537. doi: 10.1038/s41598-017-13601-y.

Gut microbiome alterations in Alzheimer's disease.

Author information

1
Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, 600 Highland Avenue J5/1 Mezzanine, Madison, WI 53792, USA.
2
Department of Bacteriology, University of Wisconsin-Madison, 1550 Linden Drive, Madison, WI 53706, USA.
3
Geriatric Research Education and Clinical Center, William S. Middleton Memorial Veterans Hospital, 2500 Overlook Terrace, Madison, WI 53705, USA.
4
Wisconsin Alzheimer's Institute, University of Wisconsin School of Medicine and Public Health, WARF Building, 610 Walnut Street, 9th Floor, Suite 957, Madison, WI 53726, USA.
5
Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
6
Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
7
Department of Molecular Neuroscience, University College London Institute of Neurology, Queen Square, London, United Kingdom.
8
UK Dementia Research Institute at University College London, London, United Kingdom.
9
Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, 600 Highland Avenue J5/1 Mezzanine, Madison, WI 53792, USA. bbb@medicine.wisc.edu.
10
Wisconsin Alzheimer's Institute, University of Wisconsin School of Medicine and Public Health, WARF Building, 610 Walnut Street, 9th Floor, Suite 957, Madison, WI 53726, USA. bbb@medicine.wisc.edu.
11
Department of Bacteriology, University of Wisconsin-Madison, 1550 Linden Drive, Madison, WI 53706, USA. ferey@wisc.edu.

Abstract

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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