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Furthermore, the protein level of p-AMPK was enhanced significantly and p-mTOR was declined, which manifested that AMPK-mTOR signaling pathway was activated in Cu-treated groups. In conclusion, this study illuminated that the accumulation of Cu could cause mitochondrial dysfunction, induce mitochondria-mediated apoptosis and activate AMPK-mTOR pathway in hypothalamus.Upregulation of the PI3K/AKT/mTOR pathway has been implicated in glioma-related epileptogenesis. In this retrospective analysis, epilepsy characteristics and response to treat
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