Deregulated MicroRNAs Associated With Alzheimer’s Disease

D. Temraz

Abstract


Alzheimer’s disease (AD) is one of the most common neurodegenerative disorders caused by aging. Alzheimer discussed his findings on the brain pathology and symptoms of presenile dementia publicly on 3 November 1906, at the Tübingen meeting of the Southwest German Psychiatrists. The attendees at this lecture seemed uninterested in what he had to say. Following the lecture, Alzheimer published a short paper summarizing his lecture; in 1907 he wrote a larger paper detailing the disease and his findings. Kraepelin first named the disease as Alzheimer's disease in Handbook of Psychiatry in the chapter on "Presenile and Senile Dementia" in 1910. Dr. Alois Alzheimer, characterized the disorder with the presence of amyloid plaques and neurofibrillary triangle (NFT) in the patient’s brain. Recently, studies exhibit that miRNA plays a role in moderating expression of the AD-related genes as well as subsequent phenotypic manifestation. Additionally, a number of studies indicate that miRNA is deregulated in AD human brain. In this review we focused on three aspects of the roles of miRNAs in the development of the Alzheimer’s disease: 1) During the progress of the disease, miRNA’s expression mutates and plays a pathological impact on the pathogenesis. Therefore, identifying and analyzing the expression of the microRNA will provide an insight on the pathogenic. 2) Since a single miRNA may have multiple gene targets in Alzheimer’s disease it is necessary to identify differently expressed miRNAs (DEM) and differently expressed genes (DEG). 3) Since miRNA’s target multiple genes through pathways, they make complex regulatory networks, and search of such networks allows better understanding and modeling the biological system of the disease.

Keywords


Alzheimer’s disease; microRNA; regulatory networks

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DOI: http://dx.doi.org/10.21533/scjournal.v6i2.141

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Copyright (c) 2018 D. Temraz

ISSN 2233 -1859

Digital Object Identifier DOI: 10.21533/scjournal

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This work is licensed under a Creative Commons Attribution 4.0 International License