Abstract:The present study is designed to investigate the possible hepatotoxic effects of the anti-epileptic drug "lamotrigine, LTG" in adult male wister rats after picrotoxin -induced convulsions and exposure for 21 days to chronic restraint model. This was done by a trial to find out alterations in the activities of liver enzymes and some antioxidants in this model of co-morbidity. They were treated by gastric gavage with LTG [20mg/kg body wt.] for 21days. Then rats were anesthetized and dissected to remove liver and to collect blood. Selected liver enzymes [AST, ALT] and some anti-oxidant enzymes were assayed. The results indicated that the drug significantly increased the activities of glutathione peroxidase and catalase enzymes in hepatic homogenates, while it significantly decreased the level of the lipid peroxidation expressed as thiobarbituric acid-reactive substance (TBARS) in these homogenates. However, there was an elevation of tested liver enzymes ALT & AST at the end of 21 days. This revealed the occurrence of possible hepatocellular damage. The present study recommends a regular liver function and drug monitoring during the therapeutic use of this drug in epilepsy-stress comorbidity.

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Alzheimer's disease (AD) are often associated with memory and cognitive deficits. Effective treatment of these diseases leads to a marked improvement in the cognitive function of such patients. There is a suggestion that there is some neuroprotective properties of duloxetine, as one of the antidepressants, against dementia-associated with cognitive disorders. The present study assessed cognitively enhancing property of duloxetine in a demented adult APP/PS1 transgenic mouse model of AD. Intraperitoneal (ip) administration of a single dose of duloxetine 10 mg/kg/day before each test. This drug treatment rescued cognitive deficits in APP/PS1 mice in both cognitive tests used in this study. The results of the present study suggest that duloxetine administration can help in improvement of cognitive disorder and may inhibit any memory impairement that accompanied the pathogenesis of AD.