**9. Conclusion**

This review highlights several key points relating to the role of AA in healthy brain aging: (1) both human and animal studies demonstrate AA deficiency in association with oxidative stress markers, and oxidative stress is a consistent observation in AD; (2) there is inconsistency among the large observational studies relating dietary intake of AA to cognition. However, it remains unclear whether this inconsistency is methodological in nature (e.g., the subjective dietary surveys used to capture AA intake) since biomarkers of both AA (and oxidative stress) present more consistent results favouring an important role for AA in cognitive health; (3) there are genetic (SVCT1 and SVCT2 SNPs) and non-genetic (e.g., age) factors that modulate AA absorption and assimilation, which could indicate an increased demand for AA in subsets of the population such as the elderly and those with an AD diagnosis. Thus, we do not suggest that AA deficiency in isolation can explain AD neuro- and psycho-pathology, however, we do propose more research focused on investigating the specific role of AA in AD pathogenesis with meticulous attention to the study design (e.g., people with low AA and high vascular risk may be best suited for intervention). This activity should provide more conclusive data on this remarkable micronutrient highly concentrated in the brain.
