The X Files: “The Mystery of X Chromosome Instability in Alzheimer’s Disease”

Vladan P. Bajic, Magbubah Essack, Lada Zivkovic, Alan Stewart, Sonja Zafirovic, Vladimir B. Bajic, Takashi Gojobori, Esma Isenovic, Biljana Spremo-Potparevic

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24 Scopus citations


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.
Original languageEnglish (US)
JournalFrontiers in Genetics
StatePublished - Jan 28 2020

Bibliographical note

KAUST Repository Item: Exported on 2020-10-01
Acknowledged KAUST grant number(s): BAS/1/1606-01-01, FCC/1/1976-17-01, OSR#4129
Acknowledgements: This 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 (EI) and No. 173034 (VPB) from the Ministry of Education, Science and Technological Development, Republic of Serbia and by the KAUST grant OSR#4129 (to EI and VBB), which also supported SZ and VPB. VBB has been supported by the KAUST Base Research Fund (BAS/1/1606-01-01), while VBB and ME have been supported by KAUST Office of Sponsored Research (OSR) grant no. FCC/1/1976-17-01. TG has been supported by the King Abdullah University of Science and Technology (KAUST) Base Research Fund (BAS/1/1059-01-01).


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