Ischemic stroke is a condition caused by an obstruction of blood flow to the brain. Traditionally, there has been a high prevalence in the aged population, but it is increasingly affecting younger adults, reshaping the traditionally understood demographics. Nutrition is a modifiable risk factor for ischemic stroke. The B-vitamin, folic acid and nutrient, choline have previously been reported to impact ischemic stroke outcomes. The aim of this review is to provide mechanistic insight into how increasing levels of folic acid or choline impact brain function after injury. Our survey of the literature has demonstrated that increasing intake of folic acid after brain injury results in reduced apoptosis and autophagy in the brain, along with diminished inflammation and oxidative stress. There is an increase in cellular proliferation and improved mitochondrial function. Whereas, increasing levels of choline also resulted in improved neurite growth post injury. Prenatal supplementation with choline alleviated Alzheimer's disease phenotype in offspring by enhancing neuronal survival and integrity; this could be applied to stroke models. In recent years, the field of stroke research has faced a reproducibility crisis, in that many preclinical studies do not translate into clinical therapies. We discuss two components of the preclinical research that need to be improved: inclusion of females and the use of model systems at the applicable age. The results of our review demonstrate that increasing dietary levels of folic acid or choline is beneficial after brain injury using model systems. As discussed above, these studies need to undergo rigorous experimental design and analysis using both male and female animals that are the age most applicable to human conditions.
Jones et al. (Thu,) studied this question.