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. 2021 Mar 15;13:641080. doi: 10.3389/fnagi.2021.641080

Figure 1.

Figure 1

Summary of the function of miRNAs in the pathogenesis of AD. (A) Expressions of miR-135b (Zhang et al., 2016b), miR-195 (Zhu et al., 2012), miR-34a-5p (Liang et al., 2020), miR-384 (Liu et al., 2014b), miR-125b-5p (Liang et al., 2020), miR-31 (Barros-Viegas et al., 2020), miR-200a-3p (Pan et al., 2019), and miR-339-5p (Long et al., 2014) are decreased in patients with Alzheimer's disease. These miRNAs bind with the 3' UTR of BACE1 and decrease its expression. Therefore, the downregulation of these miRNAs leads to the upregulation of BACE1. In addition, expression levels of some APP-binding miRNAs namely miR-101 (Vilardo et al., 2010), miR-153 (Liang et al., 2012), miR-16 (Liu et al., 2012), miR-384 (Liu et al., 2014b), miR-31 (Barros-Viegas et al., 2020), miR-193b (Liu et al., 2014a), and miR-455-3p (Kumar et al., 2019) is decreased in patients with Alzheimer's disease. (B) Tau phosphorylation leads to defects in microtubules and induction of neurofibrillary tangles which result in neuron death. miR-138 and miR-425-5p are increased in Alzheimer's disease. These miRNAs regulate the expression of GSK-3β and enhance Tau phosphorylation (Wang et al., 2015b; Yuan et al., 2020). In addition, downregulation of miR-132 and upregulation of miR-125b and miR-922 leads to Tau hyperphosphorylation (Zhao et al., 2014; Salta et al., 2016; Ma et al., 2017).