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Observational analysis shows reduced anxiety- and depression-like behaviors in METH-exposed models, suggesting FGE as a potential treatment.
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.
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Liu et al. (2026) studied this question.
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