• MicroRNAs in Alzheimer's disease (AD).
  • Ayda Khatibi,1,*
    1. Department of Biological Sciences, Faculty of Basic Sciences, University of Nabi Akram, Tabriz.


  • Introduction: Alzheimer's disease (AD) is the most prevalent form of dementia, accounting for about 70% of dementia cases. The risk of AD significantly increases after the age of 65, rising to 30% for individuals over 85 years old. The typical symptoms of Alzheimer's disease begin with episodic memory loss and then progress to cognitive and behavioral impairments. Although the underlying cause of AD remains unclear, neurological inflammation, extracellular plaques, and intracellular fibrillary neurological complexities are significant pathological markers of the disease. Accumulating evidence in AD research suggests that changes in the microRNA (miRNA) network could contribute to the disease's risk. MiRNAs are conserved small non-coding RNAs that regulate gene expression at the posttranscriptional level and are crucial for neuronal function and survival. Recent profiling experiments in humans indicate that several specific miRNAs are dysregulated in disease conditions, some of which have been implicated in the regulation of key genes involved in AD. This review aims to summarize current findings on miRNA research, providing a robust foundation for future studies seeking to understand the potential role of miRNAs in AD pathophysiology.
  • Methods: In our research, we examined articles from several reputable sources including Scopus, PubMed, Google Scholar, Civilica, and ScienceDirect. Our search terms focused on miRNA, Alzheimer's disease, and biomarkers. We specifically targeted recent articles and their respective references, ultimately selecting 96 out of 110 articles as key sources. Our search was confined to articles published in English and Persian.
  • Results: Regulating gene expression through translation control is a pivotal factor that influences the disparity between mRNA and protein levels. Clinical research data highlights the significance of amyloid-B (AB42), total tau (T-tau), and phosphorylated tau (P-tau) biomarkers in reflecting key aspects of AD pathophysiology. Variances in miRNA expression in patient tissues and their distinct enrichment in plasma, serum, and other bodily fluids have been observed, potentially indicating their utility in routine clinical diagnosis. Furthermore, studies have linked AD to platelet and vascular irregularities.
  • Conclusion: The personal and societal impact of AD poses challenges in quantification. The breadth of its effects spans multiple dimensions. Individuals diagnosed with AD encounter difficulties in recollecting daily activities and may manifest sleep and behavioral disturbances. Economically, the impact of AD is substantial and escalating. Concurrent with global population aging, the worldwide AD patient count is projected to reach 115 million by 2050. As of now, there is no definitive AD treatment, but various symptomatic therapies, including anti-cholinesterase drugs and NMDA antagonists, are available. These treatments yield temporary enhancements in cognitive functions. The aforementioned intervention goals and strategies may foster the development of novel pharmacological compounds. These compounds can be explored through various drug discovery techniques and potentially provide avenues for addressing AD, leading to the formulation of new treatment regimens for the disease.
  • Keywords: miRNA, Micro RNA, Alzheimer's disease, Biomarkers.