The X files : ''The mystery of X chromosome instability in Alzheimer's disease''
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Alzheimer’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.
Bajic , 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.2019.01368
Frontiers in Genetics
Copyright © 2020 Bajic, Essack, Zivkovic, Stewart, Zafirovic, Bajic, Gojobori, Isenovic and Spremo-Potparevic. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
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).
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