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Sökning: onr:"swepub:oai:lup.lub.lu.se:11e94b1d-0994-4543-980a-805429c583af" > Reduction of Abeta ...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003775naa a2200421 4500
001oai:lup.lub.lu.se:11e94b1d-0994-4543-980a-805429c583af
003SwePub
008170223s2017 | |||||||||||000 ||eng|
024a https://lup.lub.lu.se/record/11e94b1d-0994-4543-980a-805429c583af2 URI
024a https://doi.org/10.1038/srep418022 DOI
040 a (SwePub)lu
041 a engb eng
042 9 SwePub
072 7a art2 swepub-publicationtype
072 7a ref2 swepub-contenttype
100a Harach, T.u Swiss Federal Institute of Technology4 aut
2451 0a Reduction of Abeta amyloid pathology in APPPS1 transgenic mice in the absence of gut microbiota
264 c 2017-02-08
264 1b Springer Science and Business Media LLC,c 2017
520 a Alzheimer's disease is the most common form of dementia in the western world, however there is no cure available for this devastating neurodegenerative disorder. Despite clinical and experimental evidence implicating the intestinal microbiota in a number of brain disorders, its impact on Alzheimer's disease is not known. To this end we sequenced bacterial 16S rRNA from fecal samples of Aβ precursor protein (APP) transgenic mouse model and found a remarkable shift in the gut microbiota as compared to non-transgenic wild-type mice. Subsequently we generated germ-free APP transgenic mice and found a drastic reduction of cerebral Aβ amyloid pathology when compared to control mice with intestinal microbiota. Importantly, colonization of germ-free APP transgenic mice with microbiota from conventionally-raised APP transgenic mice increased cerebral Aβ pathology, while colonization with microbiota from wild-type mice was less effective in increasing cerebral Aβ levels. Our results indicate a microbial involvement in the development of Abeta amyloid pathology, and suggest that microbiota may contribute to the development of neurodegenerative diseases.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Neurovetenskaper0 (SwePub)301052 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Neurosciences0 (SwePub)301052 hsv//eng
700a Marungruang, N.u Lund University,Lunds universitet,Centrum för preventiv livsmedelsforskning,Universitetets särskilda verksamheter,Food for Health Science Centre,University Specialised Centres4 aut0 (Swepub:lu)appl-nym
700a Duthilleul, N.u Swiss Federal Institute of Technology4 aut
700a Cheatham, V.u Swiss Federal Institute of Technology4 aut
700a Mc Coy, K. D.u University of Bern4 aut
700a Frisoni, G. B.u Geneva University Hospital,University of Geneva4 aut
700a Neher, J. J.u German Center for Neurodegenerative Diseases (DZNE), Bonn,University of Tübingen4 aut
700a Fåk, F.u Lund University,Lunds universitet,Centrum för preventiv livsmedelsforskning,Universitetets särskilda verksamheter,Food for Health Science Centre,University Specialised Centres4 aut0 (Swepub:lu)cob-ffa
700a Jucker, Mathiasu University of Tübingen,German Center for Neurodegenerative Diseases (DZNE), Bonn4 aut
700a Lasser, Theou Swiss Federal Institute of Technology4 aut
700a Bolmont, T.u Swiss Federal Institute of Technology,Stemedica International4 aut
710a Swiss Federal Institute of Technologyb Centrum för preventiv livsmedelsforskning4 org
773t Scientific Reportsd : Springer Science and Business Media LLCg 7q 7x 2045-2322
856u http://dx.doi.org/10.1038/srep41802x freey FULLTEXT
856u https://www.nature.com/articles/srep41802.pdf
8564 8u https://lup.lub.lu.se/record/11e94b1d-0994-4543-980a-805429c583af
8564 8u https://doi.org/10.1038/srep41802

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