Non-coding RNAs and their role in Alzheimer's pathogenesis

Document Type : Narrative Review

Authors

1 Orthopedic Surgeon, Shahid Beheshti University of Medical Sciences, Tehran, Iran

2 Group of Bio-photomatiχ, Department of Information and Communication Technology, Mawlana Bhashani Science and Technology University, Santosh, Tangail-1902, Bangladesh

3 Department of Electrical and Computer Engineering, University of Saskatchewan, 57 Campus Drive, Saskatoon, SK S7N 5A9, Canada

Abstract

Alzheimer's disease is a progressive and irreversible brain disorder. This disease is the most common reason for dementia in aged people. Pathological symptoms of this disease are the formation of beta-amyloid plaques and neurofibrillary tangles. Beta-amyloid plaques appear intercellularly, while neurofibrillary tangles appear intracellularly. Defects in genes such as PSEN, APP, BACE1, etc., can cause Alzheimer's. However, some mechanisms that alter gene expression can have the main role in disease pathogenesis. One of the post-transcriptional mechanisms that can alter gene expression is the involvement of non-coding RNAs. Many kinds of non-coding RNAs exist, two of which are microRNAs and long non-coding RNAs. These can alter the expression of many genes by influencing the stability or structure of mRNAs. Non-coding RNAs can alter the risk of Alzheimer's disease if they affect genes involved in Alzheimer's pathogenesis. The mechanisms of influence of non-coding RNAs on the onset and development of Alzheimer's are not clear. This study aimed to describe the mechanisms of involvement of non-coding RNAs in the pathogenesis of Alzheimer's disease.

Graphical Abstract

Non-coding RNAs and their role in Alzheimer's pathogenesis

Highlights

  • Alzheimer's disease is a progressive and irreversible brain impairment in the elderly.
  • Beta-amyloid plaques and neurofibrillary tangles are the main pathological symptoms of Alzheimer's.
  • Non-coding RNAs could involve in the pathogenesis of Alzheimer's disease.

Keywords

Main Subjects


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