6533b85cfe1ef96bd12bc09c

RESEARCH PRODUCT

Impact of Acute and Chronic Amyloid-β Peptide Exposure on Gut Microbial Commensals in the Mouse

Malena Dos Santos GuilhermeHristo TodorovHristo TodorovHristo TodorovCarina OsterhofAnton MöllerkeKristina CubThomas HankelnSusanne GerberSusanne GerberKristina Endres

subject

Microbiology (medical)mouse modelTransgenelcsh:QR1-502microbiomeDiseaseGut floraMicrobiologylcsh:Microbiology03 medical and health sciencesIn vivomedicineMicrobiomeOriginal Research030304 developmental biologyAmyloid-β peptide0303 health sciencesanti-microbialbiology030306 microbiologyWild typebiology.organism_classificationmedicine.disease5xFADPhenotypeImmunologyAlzheimer’s diseaseDysbiosis

description

Alzheimer’s disease (AD) is the most common form of dementia. Besides its cognitive phenotype, AD leads to crucial changes in gut microbiome composition in model mice and in patients, but the reported data are still highly inconsistent. Therefore, we investigated chronic effects of AD-characteristic neurotoxic amyloid-β (Aβ) peptides as provided by transgenic overexpression (5xFAD mouse model) and acute effects due to oral application of Aβ on gut microbes. Astonishingly, one-time feeding of wild type mice with Aβ42 provoked immediate changes in gut microbiome composition (β diversity) as compared to controls. Such obvious changes were not observed when comparing 5xFAD mice with wild type littermates. However, acute as well as chronic exposure to Aβ significantly affected the abundance of numerous individual operational taxonomic units. This provides first evidence that acute in vivo exposure to Aβ results in a shift in the enteric microbiome. Furthermore, we suggest that chronic exposure to Aβ might trigger an adaptive response of gut microbiota which could thereby result in dysbiosis in model mice but also in human patients.

https://doi.org/10.3389/fmicb.2020.01008