Abstract
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.
Highlights
Alzheimer's disease, the neurological disorder in adults is corruption
Mitochondrial tRNA genes were found in 15 changes
Mutations in mitochondrial tRNA genes have been reported in various neurological diseases and the risk of developing Alzheimer's disease revealed by mitochondrial mutations
Summary
The disease, with a gradual and progressive loss of consciousness and memory show [1]. Pathogenic processes, structural and functional damage in the form of neurons, neuronal connections are in place and the physiological mechanism of cell death shows [2], for example, regulate hormones and reduce impaired cellmediated immunity and humoral immunity have been reported to increase [3]. Environmental health and psychological processes related to aging man set that led to the weakening of the nervous system in Alzheimer's disease [4]. Epidemiology studies suggest that the risk of late model, in offspring of parents with Alzheimer's disease or inherited maternally inherited mitochondrial disease, which is fully compatible with the pattern [5]. Mitochondrial DNA mutations strong opinion, caused the disease in a non-Mendelian pattern of inheritance mother who inherited [6]
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