This study demonstrates that FGE, a potential natural agent, alleviates anxiety- and depression-like behaviors induced by METH through the reduction of neuroinflammation in the hippocampus. The protective effects of FGE against METH-induced neuronal damage and behavioral deficits are likely mediated by the PI3K-AKT signaling pathway. These findings suggest FGE as a promising therapeutic strategy for METH-related neurological disorders.
Liu et al. (Tue,) studied this question.