E-vapour inhalation-How does it affect memory?

Tobacco smoking is well-known to affect cognitive behaviour, particularly short-term memory; whilst high-fat diet (HFD) consumption has similar adverse impact on cognitive behaviour. E-cigarettes gained popularity by purporting to be a safer nicotine delivery system than cigarettes (fewer toxicants and thus presumed lower cancer producing effects). However, the impact of e-vapour inhalation on cognition is unknown as is the contribution of HFD. In this study, we aimed to investigate whether e-vapour inhalation interacts with HFD to affect short-term memory function and neural integrity in a mouse model. Balb/c mice (7 weeks) were fed a HFD (43% fat, 20 kJ/g, n = 30) for 10 weeks to induce obesity with chow as control (14% fat, 14 kJ/g, n = 30). From weeks 11–16, a sub-group of mice (n = 15) in each dietary group was exposed to e-vapour (18 mg/mL nicotine, tobacco flavour) twice daily. Novel objective recognition test (NOR) was performed in week 15. Half of the brain hemisphere was collected for Western blotting for phosphorylated (p)-Tau protein level, and the other half was fixed for immunohistochemistry of the hippocampus for the apoptotic markers active caspase-3 and TUNEL. HFD consumption alone did not impair the performance during NOR, although p-Tau was reduced in the whole brain (p < 0.05), and Caspase 3 and TUNEL were increased in the hippocampus. In mice exposed to e-vapour, short-term memory function was significantly impaired, and was independent of the diet. E-vapour exposure significantly increased p-Tau levels, Caspase 3 and TUNEL positive cells in chow-fed mice but reduced p-Tau levels in HFD mice. In conclusion, long term e-vapour exposure led to impaired cognitive function independent of diet. Although HFD consumption alone increased p-Tau level and cell death, short-term memory function was not affected. There was no interaction between e-vapour exposure and HFD consumption on cognition in the current setting.