Publication:
Elevation in Sphingomyelin Synthase Activity Is Associated with Increases in Amyloid-Beta Peptide Generation

dc.contributor.author Hsiao, Jen-Hsiang T en_US
dc.contributor.author YuHong, Fu en_US
dc.contributor.author Hill, Andrew F en_US
dc.contributor.author Halliday, Glenda en_US
dc.contributor.author Woojin, Scott Kim en_US
dc.date.accessioned 2021-11-25T12:28:36Z
dc.date.available 2021-11-25T12:28:36Z
dc.date.issued 2013 en_US
dc.description.abstract A pathological hallmark of Alzheimer’s disease (AD) is the presence of amyloid-beta peptide (Aβ) plaques in the brain. Aβ is derived from a sequential proteolysis of the transmenbrane amyloid precursor protein (APP), a process which is dependent on the distribution of lipids present in the plasma membrane. Sphingomyelin is a major membrane lipid, however its role in APP processing is unclear. Here, we assessed the expression of sphingomyelin synthase (SGMS1; the gene responsible for sphingomyelin synthesis) in human brain and found that it was significantly elevated in the hippocampus of AD brains, but not in the cerebellum. Secondly, we assessed the impact of altering SGMS activity on Aβ generation. Inhibition of SGMS activity significantly reduced the level of Aβ in a dose and time dependent manner. The decrease in Aβ level occurred without changes in APP expression or cell viability. These results when put together indicate that SGMS activity impacts on APP processing to produce Aβ and it could be a contributing factor in Aβ pathology associated with AD. en_US
dc.identifier.issn 1932-6203 en_US
dc.identifier.uri http://hdl.handle.net/1959.4/53320
dc.language English
dc.language.iso EN en_US
dc.rights CC BY-NC-ND 3.0 en_US
dc.rights.uri https://creativecommons.org/licenses/by-nc-nd/3.0/au/ en_US
dc.source Legacy MARC en_US
dc.subject.other Sphingomyelin en_US
dc.subject.other amyloid-beta peptide en_US
dc.subject.other Alzheimer’s disease en_US
dc.title Elevation in Sphingomyelin Synthase Activity Is Associated with Increases in Amyloid-Beta Peptide Generation en_US
dc.type Journal Article en
dcterms.accessRights open access
dspace.entity.type Publication en_US
unsw.accessRights.uri https://purl.org/coar/access_right/c_abf2
unsw.identifier.doiPublisher http://dx.doi.org/10.1371/journal.pone.0074016 en_US
unsw.relation.FunderRefNo GNT1022325 en_US
unsw.relation.FunderRefNoURL http://purl.org/au-research/grants/nhmrc/1022325 en_US
unsw.relation.faculty Medicine & Health
unsw.relation.fundingScheme NHMRC Project en_US
unsw.relation.ispartofissue 8 en_US
unsw.relation.ispartofjournal PLoS ONE en_US
unsw.relation.ispartofpagefrompageto e74016 en_US
unsw.relation.ispartofvolume 8 en_US
unsw.relation.originalPublicationAffiliation Hsiao, Jen-Hsiang T en_US
unsw.relation.originalPublicationAffiliation YuHong, Fu en_US
unsw.relation.originalPublicationAffiliation Hill, Andrew F en_US
unsw.relation.originalPublicationAffiliation Halliday, Glenda, Medical Sciences, Faculty of Medicine, UNSW en_US
unsw.relation.originalPublicationAffiliation Woojin, Scott Kim, Medical Sciences, Faculty of Medicine, UNSW en_US
unsw.relation.school School of Medical Sciences *
unsw.subject.fieldofresearchcode 110903 Central Nervous System en_US
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