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dc.contributor.authorBajic, Vladan P.
dc.contributor.authorEssak, Mugbubah
dc.contributor.authorZivkovic, Lada
dc.contributor.authorStewart, Alan
dc.contributor.authorZafirovic, Sonja
dc.contributor.authorBajic, Vladimir
dc.contributor.authorGojobori, Takashi
dc.contributor.authorIsenovic, Esma
dc.contributor.authorSpremo-Potparevic, Biljana
dc.date.accessioned2020-01-28T12:30:05Z
dc.date.available2020-01-28T12:30:05Z
dc.date.issued2020-01-28
dc.identifier264359107
dc.identifier8b3a886c-1d7b-4041-98f9-8faf3efc9cf7
dc.identifier85079496526
dc.identifier000514292900001
dc.identifier.citationBajic , V P , Essak , M , Zivkovic , L , Stewart , A , Zafirovic , S , Bajic , V , Gojobori , T , Isenovic , E & Spremo-Potparevic , B 2020 , ' The X files : ''The mystery of X chromosome instability in Alzheimer's disease'' ' , Frontiers in Genetics , vol. 10 , 1368 . https://doi.org/10.3389/fgene.2019.01368en
dc.identifier.issn1664-8021
dc.identifier.urihttps://hdl.handle.net/10023/19362
dc.descriptionThis work is part of the collaboration between the Laboratory of Radiobiology and Molecular Genetics, Vinca Institute of Nuclear Sciences, University of Belgrade, Belgrade, Serbia and King Abdullah University of Science and Technology (KAUST), Computational Bioscience Research Center (CBRC), Thuwal, Saudi Arabia. This work has been supported by grants No. 173033 (E.R.I.) and No. 173034 (V.P.B) from the Ministry of Education, Science and Technological Development, Republic of Serbia and by the KAUST grant OSR#4129 (to E.R.I. and V.B.B.), which also supported S.Z. and V.P.B.; V.B.B. has been supported by the KAUST Base Research Fund (BAS/1/1606-01-01), while V.B.B. and M.E. have been supported by KAUST Office of Sponsored Research (OSR) grant no. FCC/1/1976-17-01. T.G. has been supported by the King Abdullah University of Science and Technology (KAUST) Base Research Fund (BAS/1/1059-01-411 01).en
dc.description.abstractAlzheimer’s disease (AD) is a neurodegenerative disease that affects millions of individuals worldwide and can occur relatively early or later in life. It is well known that genetic components, such as the amyloid precursor protein gene on chromosome 21, are fundamental in early-onset AD (EOAD). To date, however, only the apolipoprotein E4 (ApoE4) gene has been proved to be a genetic risk factor for late-onset AD (LOAD). In recent years, despite the hypothesis that many additional unidentified genes are likely to play a role in AD development, it is surprising that additional gene polymorphisms associated with LOAD have failed to come to light. In this review, we examine the role of X chromosome epigenetics and, based upon GWAS studies, the PCDHX11 gene. Furthermore, we explore other genetic risk factors of AD that involve X-chromosome epigenetics.
dc.format.extent11
dc.format.extent672608
dc.language.isoeng
dc.relation.ispartofFrontiers in Geneticsen
dc.subjectX chromosomeen
dc.subjectAlzheimer's diseaseen
dc.subjectSex chromosome dosageen
dc.subjectProtocadherin 11en
dc.subjectCentromere instabiilityen
dc.subjectQH426 Geneticsen
dc.subject.lccQH426en
dc.titleThe X files : ''The mystery of X chromosome instability in Alzheimer's disease''en
dc.typeJournal itemen
dc.contributor.institutionUniversity of St Andrews. Sir James Mackenzie Institute for Early Diagnosisen
dc.contributor.institutionUniversity of St Andrews. Cellular Medicine Divisionen
dc.contributor.institutionUniversity of St Andrews. Biomedical Sciences Research Complexen
dc.contributor.institutionUniversity of St Andrews. Institute of Behavioural and Neural Sciencesen
dc.contributor.institutionUniversity of St Andrews. School of Medicineen
dc.identifier.doi10.3389/fgene.2019.01368
dc.description.statusPeer revieweden
dc.date.embargoedUntil2020-01-28


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