Previous research has suggested that AMPK activation can increase the expression of BDNF, which plays a vital role in the maintenance of synaptic plasticity and depression/anti-depression by activating CREB and Akt/GSK3 signaling pathways [206] and mTOR signaling [207], and by regulating DNA hydroxymethylation via the AMPK/Tet2 pathway [204]. The gene discussed is MTOR; the disease is depressive symptom measurement.