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In Silico Analysis of Single Nucleotide Polymorphisms (SNPS) in Human Abetalipoprotein Epsilon 4 (APOE E4) Gene as a Cause of Alzheimer’s Disease from Genetic Mutation to Functional Predication from Structural Change Patterns

Author

Listed:
  • Abdelmohymin AA Abdalla
  • Mohamed Elsheikh
  • Ahmed Babiker
  • Mohanad Abdelrahim
  • Mohamed Abdelrahim
  • Mohamed Taha
  • Mohamed Muneer
  • Mahil Abdalla
  • Mohamedahamed Hassan Author-NameAbbashar Hussein

    (Department of Bioinformatics, University of Khartoum, Sudan)

Abstract

Alzheimer disease (AD) is an acquired disorder of cognitive and behavioral impairment that markedly interferes with social and occupational functioning. Single-nucleotide polymorphisms (SNPs) play a major role in the understanding of the genetic basis of this complex disease. In this work, we have analyzed the genetic variation that can alter the expression and the function of the APOE e4 gene by analysing the SNPs in the coding regions of APOE e4 gene using computational methods. Genomic analysis of APOE e4 was initiated Polyphen and SIFT server used to retrieve 10 harmful mutations, among of these nsSNPs damaged SNPs six non-synonymous SNPs showed very damaging by higher PSIC score of the Polyphen server with a SIFT tolerance index of 0.00-0.01 (R50C, L115S, R132S, E139V, E150G, R168H); and one in very highly conserve region (R154P). Screening for these SNPs variants in coding region may help in Alzheimer disease molecular and genetic early diagnosis.

Suggested Citation

  • Abdelmohymin AA Abdalla & Mohamed Elsheikh & Ahmed Babiker & Mohanad Abdelrahim & Mohamed Abdelrahim & Mohamed Taha & Mohamed Muneer & Mahil Abdalla & Mohamedahamed Hassan Author-NameAbbashar Hussein, 2017. "In Silico Analysis of Single Nucleotide Polymorphisms (SNPS) in Human Abetalipoprotein Epsilon 4 (APOE E4) Gene as a Cause of Alzheimer’s Disease from Genetic Mutation to Functional Predication from," Current Trends in Biomedical Engineering & Biosciences, Juniper Publishers Inc., vol. 5(1), pages 10-17, May.
    • Handle: RePEc:adp:jctbeb:v:5:y:2017:i:1:p:10-17
    DOI: 10.19080/CTBEB.2017.05.555653
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