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Studies have shown that exenatide treatment promotes insulin signaling pathways in the brain, manifested as increased tyrosine phosphorylation of insulin receptor substrate 1 and increased expression of downstream Akt and phosphorylated mTOR [169]

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Therefore, the greater reduction in escape latency among younger animals could be due to their inherently higher baseline synaptic plasticity and neuronal signaling pathways, which are more amenable to enhancement by 1-MX

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