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dc.contributor.authorLeskelä, S
dc.contributor.authorTakalo, M
dc.contributor.authorMarttinen, M
dc.contributor.authorHuber, N
dc.contributor.authorPaananen, J
dc.contributor.authorMitra, V
dc.contributor.authorRauramaa, T
dc.contributor.authorMäkinen, P
dc.contributor.authorLeinonen, V
dc.contributor.authorSoininen, H
dc.contributor.authorPike, I
dc.contributor.authorRemes, AM
dc.contributor.authorHiltunen, M
dc.contributor.authorHaapasalo, A
dc.date.accessioned2018-05-16T08:44:40Z
dc.date.available2018-05-16T08:44:40Z
dc.date.issued2018
dc.identifier.urihttps://erepo.uef.fi/handle/123456789/6602
dc.description.abstractA subset of C9orf72 repeat expansion-carrying frontotemporal dementia patients display an Alzheimer-like decrease in cerebrospinal fluid amyloid-β (Aβ) biomarker levels. We report that downregulation of C9orf72 in non-neuronal human cells overexpressing amyloid-β protein precursor (AβPP) resulted in increased levels of secreted AβPP fragments and Aβ, while levels of AβPP or its C-terminal fragments (CTFs) remained unchanged. In neuronal cells, AβPP and C83 CTF levels were decreased upon C9orf72 knockdown, but those of secreted AβPP fragments or Aβ remained unchanged. C9orf72 protein levels significantly increased in human brain with advancing neurofibrillary pathology and positively correlated with brain Aβ42 levels. Our data suggest that altered C9orf72 levels may lead to cell-type specific alterations in AβPP processing, but warrant further studies to clarify the underlying mechanisms.
dc.language.isoEN
dc.publisherIOS Press
dc.relation.ispartofseriesJournal of Alzheimer's Disease
dc.relation.urihttp://dx.doi.org/10.3233/JAD-170362
dc.rightsAll rights reserved
dc.subjectAlzheimer's disease
dc.subjectamyloid-β
dc.subjectamyloid-β protein precursor
dc.subjectC9orf72
dc.subjectfrontotemporal dementia
dc.titleInterrelationship between the Levels of C9orf72 and Amyloid-ß Protein Precursor and Amyloid-ß in Human Cells and Brain Samples
dc.description.versionfinal draft
dc.contributor.departmentA.I. Virtanen -instituutti
dc.contributor.departmentSchool of Medicine / Clinical Medicine,School of Medicine / Biomedicine
uef.solecris.id52723967en
dc.type.publicationTieteelliset aikakauslehtiartikkelit
dc.rights.accessrights© IOS Press and the authors
dc.relation.projectidinfo:eu-repo/grantAgreement/EC/FP7-ICT/601055/EU/VPH Dementia Research Enabled by IT/VPH-DARE@IT
dc.relation.projectidinfo:eu-repo/grantAgreement/EC/FP7-PEOPLE/301220/EU/Understanding the evolutionary mechanisms of invasion success: Selective footprints in the genome of an E
dc.relation.doi10.3233/JAD-170362
dc.description.reviewstatuspeerReviewed
dc.format.pagerange269-278
dc.publisher.countryAlankomaat
dc.relation.issn1387-2877
dc.relation.issue1
dc.relation.volume62
dc.rights.accesslevelopenAccess
dc.type.okmA1
uef.solecris.openaccessEi


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