alexa Twenty Two New Mutations in Mitochondrial tRNA Genes in
ISSN: 1747-0862

Journal of Molecular and Genetic Medicine
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Research Article

Twenty Two New Mutations in Mitochondrial tRNA Genes in Patients with Alzheimer's Tabriz, Iran

Shahin Asadi*, Ali Nazirzadeh and Saeideh Habibi

Islamic Azad University, Tabriz, Iran

Corresponding Author:
Shahin Asadi
Islamic Azad University
Tabriz, Iran
Tel: 984134474829
E-mail:[email protected]

Received date: October 20, 2015 Accepted date: December 18, 2015 Published date: December 20, 2015

Citation:Asadi S, Nazirzadeh, Habibi S (2015) Twenty Two New Mutations in Mitochondrial tRNA Genes in Patients with Alzheimer's Tabriz, Iran. J Mol Genet Med 9:192. doi:10.4172/1747-0862.1000192

Copyright: © 2015 Asadi S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



Alzheimer's disease is the main form of memory, and memory loss in the elderly is the interplay of genes and environment play a role in its formation. The role of mitochondrial mutations in various neurological diseases, has effectively proven that some of these mutations of Alzheimer's disease in a non-Mendelian maternal mode of inheritance that are inherited. All mitochondrial tRNA genes in 24 patients and 50 healthy controls using nucleotide sequences, was tested. Mitochondrial tRNA genes were found in fifteen change. The polymorphisms were eleven of them. Four changes T1633A, C1631A (in tRNA parents), T14723T, Q14704C, were classified as pathogenic mutations, such as heteroplasmy observed in patients, mutations of nucleotide sequences in different organisms has been identified. Polymorphism A12308G, eight patients were found in tRNA leucine. This change in various neurological diseases, as well as control samples has been reported. We believe that these changes may influence the pathogenesis of Alzheimer's disease or the disease process act as a secondary injury. The percentage of heteroplasmy may be involved in the development of symptoms or onset of the disease.


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