Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-25
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dc.contributor.authorSantos Guilherme, Malena dos-
dc.contributor.authorStoye, Nicolai M.-
dc.contributor.authorRose-John, Stefan-
dc.contributor.authorGarbers, Christoph-
dc.contributor.authorFellgiebel, Andreas-
dc.contributor.authorEndres, Kristina-
dc.date.accessioned2020-01-27T13:03:22Z-
dc.date.available2020-01-27T14:03:22Z-
dc.date.issued2019-
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/27-
dc.description.abstractThese days, the important role of retinoids in adult brain functionality and homeostasis is well accepted and has been proven by genomic as well as non-genomic mechanisms. In the healthy brain, numerous biological processes, e.g., cell proliferation, neurogenesis, dendritic spine formation as well as modulation of the immune system, have been attributed to retinoid signaling. This, together with the finding that retinoid metabolism is impaired in Alzheimer’s disease (AD), led to preclinical and early clinical testing of natural and synthetic retinoids as innovative pharmaceuticals with multifactorial properties. Acitretin, an aromatic retinoid, was found to exert an anti-amyloidogenic effect in mouse models for AD as well as in human patients by stimulating the alpha-secretase ADAM10. The lipophilic drug was already demonstrated to easily pass the blood brain barrier after i.p. administration and evoked increased nest building capability in the 5xFAD mouse model. Additionally, we analyzed the immune-modulatory capacity of acitretin via a multiplex array in the 5xFAD mouse model and evaluated some of our findings in human CSF derived from a pilot study using acitretin. Although several serum analytes did not display changes, Interleukin-6 (IL-6) was found to be significantly increased in both—mouse and human neural material. This demonstrates that acitretin exerts an immune stimulatory effect—besides the alpha-secretase induction—which could Impact the alleviation of learning and memory disabilities observed in the mouse model.en_GB
dc.description.sponsorshipDFG, Open Access-Publizieren Universität Mainz / Universitätsmedizin-
dc.language.isoeng-
dc.rightsCC BYde_DE
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/-
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleThe synthetic retinoid acitretin increases IL-6 in the central nervous system of Alzheimer disease model mice and human patientsen_GB
dc.typeZeitschriftenaufsatzde_DE
dc.identifier.urnurn:nbn:de:hebis:77-publ-595246-
dc.identifier.doihttp://doi.org/10.25358/openscience-25-
jgu.type.dinitypearticle-
jgu.type.versionPublished versionen_GB
jgu.type.resourceText-
jgu.organisation.departmentFB 04 Medizin-
jgu.organisation.number2700-
jgu.organisation.nameJohannes Gutenberg-Universität Mainz-
jgu.rights.accessrightsopenAccess-
jgu.journal.titleFrontiers in aging neuroscience-
jgu.journal.volume11-
jgu.pages.alternativeArt. 182-
jgu.publisher.year2019-
jgu.publisher.nameFrontiers Research Foundation-
jgu.publisher.placeLausanne-
jgu.publisher.urihttp://dx.doi.org/10.3389/fnagi.2019.00182-
jgu.publisher.issn1663-4365-
jgu.organisation.placeMainz-
jgu.subject.ddccode610-
opus.date.accessioned2020-01-27T13:03:22Z-
opus.date.modified2020-02-07T08:28:19Z-
opus.date.available2020-01-27T14:03:22-
opus.subject.dfgcode00-000-
opus.organisation.stringFB 04: Medizin: Klinik für Psychiatrie und Psychotherapiede_DE
opus.identifier.opusid59524-
opus.institute.number0472-
opus.metadataonlyfalse-
opus.type.contenttypeKeinede_DE
opus.type.contenttypeNoneen_GB
opus.affiliatedFellgiebel, Andreas-
opus.affiliatedEndres, Kristina-
jgu.publisher.doi10.3389/fnagi.2019.00182
jgu.organisation.rorhttps://ror.org/023b0x485
Appears in collections:JGU-Publikationen

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