Gut microbiome alterations in Alzheimer's disease.

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

Journal: Scientific reports 2019;7(1):13537

PMID: 29051531

Plain Language Summary

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Research into what causes Alzheimer’s Disease (AD) is on-going, including a proposal for a potential role of human bacterial profiles. This cross-sectional study of 25 patients diagnosed with AD and 25 individuals with no AD diagnosis (matched for age, sex, ethnicity, BMI and diabetes status) aimed to compare the gut microbiome between AD and non-AD states using faecal samples. The researchers found that the gut microbiome of the AD patients was less diverse and compositionally distinct from the age-matched control group. In particular, the AD group had decreased Firmicutes and Bifidobacterium and increased Bacteriodetes compared with control. This small study suggests therefore that the gut microbiome may be a target for therapeutic manipulation when working with patients with AD.

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.

Address: 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.; Department of Bacteriology, University of Wisconsin-Madison, 1550 Linden Drive, Madison, WI 53706, USA.; 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.; Geriatric Research Education and Clinical Center, William S. Middleton Memorial Veterans Hospital, 2500 Overlook Terrace, Madison, WI 53705, USA.; 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.; 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.; Geriatric Research Education and Clinical Center, William S. Middleton Memorial Veterans Hospital, 2500 Overlook Terrace, Madison, WI 53705, USA.; Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.; Department of Molecular Neuroscience, University College London Institute of Neurology, Queen Square, London, United Kingdom.; UK Dementia Research Institute at University College London, London, United Kingdom.; Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.; 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. [email protected].; 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. [email protected].; Department of Bacteriology, University of Wisconsin-Madison, 1550 Linden Drive, Madison, WI 53706, USA. [email protected].
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