**4. Discussion**

The purpose of this review was to examine the effect of Vitamin E in slowing down cognitive decline in MCI. Some evidence from our literature synthesis points to the putative role of Vitamin E in slowing down MCI progression to dementia. Overall, the review collectively demonstrated through analysis of various experimental studies in rats, mice, and animals and cross-sectional, case-control, prospective cohort, experimental, clinical, and double-blind randomized in human that Vitamin E has some neuroprotective effect in slowing down progression to dementia. One clinical study carried out to lower the effect of cisplatin chemotherapy neurotoxicity, the supplementation with vitamin E (alpha tocopherol) has shown lower level of neurotoxicity, which indicates that vitamin E plays a neuroprotective role [42] even when the cause of neurotoxicity could be other than mild cognitive impairment. The findings of Gugliandolo et al. (2017) have reported similar physiological responses of Vitamin E on MCI [43–45]. Another study by Kaneai et al., indicated that vitamin E offers some neuroprotective benefits by improving neurotransmission [45]. Presently, no medication can treat, prevent, or slow the progression of MCI to dementia. However, it is important to explore the role of vitamins and antioxidants in reducing or delaying to the process of cognitive decline in people with MCI [17]. Studies show that high plasma Vitamin E levels have been associated with better cognitive performance in both ageing populations, dementia, and AD patients [42,43].

Consistent to previous studies it is understood that Vitamin E might have some therapeutic role when it comes to MCI and its progression to dementia. Since several studies in human as well as in rats and mice were MCI associated with lower level of tocopherol. Thus, it may be considered a good practice to maintain Vitamin E level through dietary sources. Vitamin E can also lead to toxicity that can be fatal in some cases which warrants careful monitoring of its levels in the aging population. The guidelines on the

safe dose of vitamin E varies from 800–2000 IU/day as reported by previous studies [46,47]. Therefore, these findings should be considered rather carefully to prevent any toxic effects of vitamin E. In the meanwhile, more randomized controlled trials to further elucidate the role of Vitamin E on MCI must be conducted with larger sample sizes. Even though there are mixed results they favor a potential neuroprotective effect of Vitamin E in MCI. It would be recommended for clinical practice that the Vitamin E levels be checked annually in the elderly, and they should be provided Vitamin E supplementation in maintaining its adequate level.
