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the two conditions share common pathogenic mechanisms and influence each other Excessive glutamate release and activation of glutamate receptors promotes glioma growth, cell death and epileptic activity GABAergic signalling is antiproliferative, whereas chloride accumulation is required for mitosis and migration of tumour cells, and is responsible for epileptogenic depolarizing GABAergic activity in neurons The molecular target of rapamycin (mTOR) signalling pathway and epigenetic abnormalities are also involved in epileptogenesis and tumour growth As a result of the shared pathogenic mechanisms, antiepileptic drugs can have antitumour effects, and antitumour therapy can control seizures Single drug therapies targeting the shared mechanisms are now being assessed for combined seizure and tumour control, and have the advantage of lower risks of adverse effects and drug interactions Abstract Epilepsy often develops in patients with glioma, and the two conditions share common pathogenic mechanisms

3 Although no studies have prospectively stratified patients by baseline A1C in evaluation of the A1C-lowering efficacy of a DPP-4 inhibitor or SGLT2 inhibitor, post-hoc subgroup analyses have shown that the efficacy of SGLT2 inhibitors is greater than that of DPP-4 inhibitors among patients with higher baseline A1C ( 8-8.5%), while patients with baseline A1C at the lower end of the spectrum ( 30 mL/min and clinical CV disease according to Diabetes Canada

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