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Genetic underpinnings in Alzheimer’s disease – a review

Ein Erratum zu diesem Artikel finden Sie hier: https://doi.org/10.1515/revneuro-2018-0081
  • Ahmed A. Moustafa EMAIL logo , Mubashir Hassan , Doaa H. Hewedi , Iman Hewedi , Julia K. Garami , Hany Al Ashwal , Nazar Zaki , Sung-Yum Seo , Vassilis Cutsuridis , Sergio L. Angulo , Joman Y. Natesh , Mohammad M. Herzallah , Dorota Frydecka , Błażej Misiak , Mohamed Salama , Wael Mohamed , Mohamad El Haj und Michael Hornberger
Veröffentlicht/Copyright: 26. September 2017

Abstract

In this review, we discuss the genetic etiologies of Alzheimer’s disease (AD). Furthermore, we review genetic links to protein signaling pathways as novel pharmacological targets to treat AD. Moreover, we also discuss the clumps of AD-m ediated genes according to their single nucleotide polymorphism mutations. Rigorous data mining approaches justified the significant role of genes in AD prevalence. Pedigree analysis and twin studies suggest that genetic components are part of the etiology, rather than only being risk factors for AD. The first autosomal dominant mutation in the amyloid precursor protein (APP) gene was described in 1991. Later, AD was also associated with mutated early-onset (presenilin 1/2, PSEN1/2 and APP) and late-onset (apolipoprotein E, ApoE) genes. Genome-wide association and linkage analysis studies with identified multiple genomic areas have implications for the treatment of AD. We conclude this review with future directions and clinical implications of genetic research in AD.

Acknowledgments

HAA and NZ are funded by the United Arab Emirates University (CIT 31T085 Fund). MH is funded by Alzheimer’s Research UK and Wellcome Trust.

  1. Conflict of interest statement: The authors have no conflict of interest to declare.

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Received: 2017-05-22
Accepted: 2017-06-10
Published Online: 2017-09-26
Published in Print: 2017-12-20

©2018 Walter de Gruyter GmbH, Berlin/Boston

Heruntergeladen am 31.12.2025 von https://www.degruyterbrill.com/document/doi/10.1515/revneuro-2017-0036/html
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