Alzheimer's disease in the gut : major changes in the gut of 5xFAD model mice with ApoA1 as potential key player

dc.contributor.authorStoye, Nicolai M.
dc.contributor.authorSantos Guilherme, Malena dos
dc.contributor.authorEndres, Kristina
dc.date.accessioned2021-07-05T08:30:53Z
dc.date.available2021-07-05T08:30:53Z
dc.date.issued2020
dc.description.abstractAlzheimer's disease (AD) affects around 33 million people worldwide, which makes it the most prominent form of dementia. The main focus of AD research has been on the central nervous system (CNS) for long, but in recent years, the gut gained more attention. The intestinal tract is innervated by the enteric nervous system (ENS), built of numerous different types of neurons showing great similarity to neurons of the CNS. It already has been demonstrated that the amyloid precursor protein, which plays a major role in AD pathology, is also expressed in these cells. We analyzed gut tissue of AD model mice (5xFAD) and the respective wild-type littermates at different pathological stages: pre-pathological, early pathological and late pathological. Our results show significant difference in function of the intestine of 5xFAD mice as compared to wild-type mice. Using a pathway array detecting 84 AD-related gene products, we found ApoA1 expression significantly altered in colon tissue of 5xFAD mice. Furthermore, we unveil ApoA1's beneficial impact on cell viability and calcium homeostasis of cultured enteric neurons of 5xFAD animals. With this study, we demonstrate that the intestine is altered in AD-like pathology and that ApoA1 might be one key player within the gut.en_GB
dc.identifier.doihttp://doi.org/10.25358/openscience-6167
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/6176
dc.language.isoengde
dc.rightsCC-BY-NC-4.0*
dc.rights.urihttps://creativecommons.org/licenses/by-nc/4.0/*
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleAlzheimer's disease in the gut : major changes in the gut of 5xFAD model mice with ApoA1 as potential key playeren_GB
dc.typeZeitschriftenaufsatzde
jgu.journal.issue9de
jgu.journal.titleThe FASEB journalde
jgu.journal.volume34de
jgu.organisation.departmentFB 04 Medizinde
jgu.organisation.nameJohannes Gutenberg-Universität Mainz
jgu.organisation.number2700
jgu.organisation.placeMainz
jgu.organisation.rorhttps://ror.org/023b0x485
jgu.pages.end11899de
jgu.pages.start11883de
jgu.publisher.doi10.1096/fj.201903128RR
jgu.publisher.issn1530-6860de
jgu.publisher.nameWileyde
jgu.publisher.placeHoboken, NJde
jgu.publisher.urihttps://doi.org/10.1096/fj.201903128RRde
jgu.publisher.year2020
jgu.rights.accessrightsopenAccess
jgu.subject.ddccode610de
jgu.type.dinitypeArticleen_GB
jgu.type.resourceTextde
jgu.type.versionPublished versionde

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