Gut microbiome alterations in preclinical Alzheimer’s disease

<h4>Background</h4> Although some human studies have reported gut microbiome changes in individuals with Alzheimer’s disease (AD) dementia or mild cognitive impairment (MCI), gut microbiome alterations in preclinical AD, i.e., cerebral amyloidosis without cognitive impairment, is largely...

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Main Authors: Joon Hyung Jung, Gihyeon Kim, Min Soo Byun, Jun Ho Lee, Dahyun Yi, Hansoo Park, Dong Young Lee
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2022-01-01
Series:PLoS ONE
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9707757/?tool=EBI
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author Joon Hyung Jung
Gihyeon Kim
Min Soo Byun
Jun Ho Lee
Dahyun Yi
Hansoo Park
Dong Young Lee
author_facet Joon Hyung Jung
Gihyeon Kim
Min Soo Byun
Jun Ho Lee
Dahyun Yi
Hansoo Park
Dong Young Lee
author_sort Joon Hyung Jung
collection DOAJ
description <h4>Background</h4> Although some human studies have reported gut microbiome changes in individuals with Alzheimer’s disease (AD) dementia or mild cognitive impairment (MCI), gut microbiome alterations in preclinical AD, i.e., cerebral amyloidosis without cognitive impairment, is largely unknown. <h4>Objective</h4> We aimed to identify gut microbial alterations associated with preclinical AD by comparing cognitively normal (CN) older adults with cerebral Aβ deposition (Aβ+ CN) and those without cerebral Aβ deposition (Aβ− CN). <h4>Methods</h4> Seventy-eight CN older participants (18 Aβ+ CN and 60 Aβ− CN) were included, and all participants underwent clinical assessment and Pittsburg compound B–positron emission tomography. The V3–V4 region of the 16S rRNA gene of genomic DNA extracted from feces was amplified and sequenced to establish the microbial community. <h4>Results</h4> Generalized linear model analysis revealed that the genera Megamonas (B = 3.399, q<0.001), Serratia (B = 3.044, q = 0.005), Leptotrichia (B = 5.862, q = 0.024) and Clostridium (family Clostridiaceae) (B = 0.788, q = 0.034) were more abundant in the Aβ+ CN group than the Aβ− CN group. In contrast, genera CF231 (B = −3.237, q< 0.001), Victivallis (B = −3.447, q = 0.004) Enterococcus (B = −2.044, q = 0.042), Mitsuokella (B = −2.119, q = 0.042) and Clostridium (family Erysipelotrichaceae) (B = −2.222, q = 0.043) were decreased in Aβ+ CN compared to Aβ− CN. Notably, the classification model including the differently abundant genera could effectively distinguish Aβ+ CN from Aβ− CN (AUC = 0.823). <h4>Conclusion</h4> Our findings suggest that specific alterations of gut bacterial taxa are related to preclinical AD, which means these changes may precede cognitive decline. Therefore, examining changes in the microbiome may be helpful in preclinical AD screening.
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spelling doaj.art-d21a79f159974e4591434f7a067995102022-12-22T04:36:16ZengPublic Library of Science (PLoS)PLoS ONE1932-62032022-01-011711Gut microbiome alterations in preclinical Alzheimer’s diseaseJoon Hyung JungGihyeon KimMin Soo ByunJun Ho LeeDahyun YiHansoo ParkDong Young Lee<h4>Background</h4> Although some human studies have reported gut microbiome changes in individuals with Alzheimer’s disease (AD) dementia or mild cognitive impairment (MCI), gut microbiome alterations in preclinical AD, i.e., cerebral amyloidosis without cognitive impairment, is largely unknown. <h4>Objective</h4> We aimed to identify gut microbial alterations associated with preclinical AD by comparing cognitively normal (CN) older adults with cerebral Aβ deposition (Aβ+ CN) and those without cerebral Aβ deposition (Aβ− CN). <h4>Methods</h4> Seventy-eight CN older participants (18 Aβ+ CN and 60 Aβ− CN) were included, and all participants underwent clinical assessment and Pittsburg compound B–positron emission tomography. The V3–V4 region of the 16S rRNA gene of genomic DNA extracted from feces was amplified and sequenced to establish the microbial community. <h4>Results</h4> Generalized linear model analysis revealed that the genera Megamonas (B = 3.399, q<0.001), Serratia (B = 3.044, q = 0.005), Leptotrichia (B = 5.862, q = 0.024) and Clostridium (family Clostridiaceae) (B = 0.788, q = 0.034) were more abundant in the Aβ+ CN group than the Aβ− CN group. In contrast, genera CF231 (B = −3.237, q< 0.001), Victivallis (B = −3.447, q = 0.004) Enterococcus (B = −2.044, q = 0.042), Mitsuokella (B = −2.119, q = 0.042) and Clostridium (family Erysipelotrichaceae) (B = −2.222, q = 0.043) were decreased in Aβ+ CN compared to Aβ− CN. Notably, the classification model including the differently abundant genera could effectively distinguish Aβ+ CN from Aβ− CN (AUC = 0.823). <h4>Conclusion</h4> Our findings suggest that specific alterations of gut bacterial taxa are related to preclinical AD, which means these changes may precede cognitive decline. Therefore, examining changes in the microbiome may be helpful in preclinical AD screening.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9707757/?tool=EBI
spellingShingle Joon Hyung Jung
Gihyeon Kim
Min Soo Byun
Jun Ho Lee
Dahyun Yi
Hansoo Park
Dong Young Lee
Gut microbiome alterations in preclinical Alzheimer’s disease
PLoS ONE
title Gut microbiome alterations in preclinical Alzheimer’s disease
title_full Gut microbiome alterations in preclinical Alzheimer’s disease
title_fullStr Gut microbiome alterations in preclinical Alzheimer’s disease
title_full_unstemmed Gut microbiome alterations in preclinical Alzheimer’s disease
title_short Gut microbiome alterations in preclinical Alzheimer’s disease
title_sort gut microbiome alterations in preclinical alzheimer s disease
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9707757/?tool=EBI
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