Skip to main content
Fig. 11 | Translational Neurodegeneration

Fig. 11

From: Melatonin ameliorates tau-related pathology via the miR-504-3p and CDK5 axis in Alzheimer’s disease

Fig. 11

Melatonin attenuates tau hyperphosphorylation via the miR-504-3p/CDK5/p39 axis in AD. Under normal conditions (left), melatonin increases the expression of miR-504-3p, which targets p39 and inhibits the activity of CDK5, resulting in physiological phosphorylation of tau. In AD (right), loss of melatonin leads to downregulation of miR-504-3p expression and overexpression of p39, which promotes the interaction between p39 and CDK5. Furthermore, activation of CDK5 ultimately promotes tau hyperphosphorylation and tau-related pathology in the AD brain

Back to article page