https://www.selleckchem.com/Bcl-2.html
The knockdown of miR-485-3p in SH-SY5Y and BV2 cells was found to significantly reverse the effect of Aβ treatment on neuronal viability and neuroinflammation. AKT3 was determined as a target of miR-485-3p, which might mediate the biological function of miR-485-3p in AD pathogenesis. All the data indicated that increased serum miR-485-3p serves as a diagnostic biomarker in AD patients, and knockdown of miR-485-3p exerts a neuroprotective role by improving neuronal viability and weakening neuroinflammation, which may be mediated by AKT3. This study
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