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Alzheimer's disease (AD) is the most common progressive neurodegenerative disease associated with advanced age. It is characterized by cognitive decline and memory loss and accounts for most cases of dementia in older people. AD can be rooted in genetic, epigenetic, or environmental causes. No drugs or other therapeutic agents prevent or delay AD progression. MicroRNAs (miRNAs) are short and uncoded RNAs that can bind to 200 RNAs approximately. By inhibiting or destroying specific messenger RNAs (mRNAs), they control gene expression and broadly affect cellular functions. MiRNAs play important roles in regulating neuronal growth, neuronal differentiation, dendritic spine morphology, and synaptic flexibility in the nervous system. The expression levels of miRNAs are changed in neurological diseases, including AD, suggesting that they play an essential role in the pathogenesis of the disease. Therefore, targeting disrupted miRNAs may be a novel therapeutic approach against AD and offers multiple solutions, including harnessing the beneficial effects of beta-amyloid, reducing tau protein, reducing neuronal cell death, and protecting synapses in AD.
Shademan et al. (Thu,) studied this question.