Influence of Dietary Folic Acid, Protein, and Physical Activity upon Plasma Homocysteine, Neurocognitive Behavior, and Biomarkers of Inflammation (CRP), Angiogenesis (VEGF), and Apoptosis (Caspase-3) in CB57 Mice

Abstract

Folic acid supplementation, dietary protein, and physical activity all impact severity of chronic disease. It’s established that folic acid deficiency significantly shortens nerve lengths of hippocampal locus coeruleus cells. To further evaluate neurocognition during chronic disease, the impact of folic acid and/or protein upon oncogenic biomarkers (CRP, VEGF, and Caspase-3) after mice were exercised was assessed, and an analysis of the microbiome conducted. Evaluation of neurodegeneration observed under these conditions may reflect similar neural pathogenesis of cancer by using measurements of the ability of a mouse to build a nest, and, the amount of curiosity displayed by distance explored during an Open Field Test. Five different diets were provided: Normal Folic Acid Protein (NFC); Folic Acid Deficient (FAD); Folic Acid Supplemented (FAS); Low Protein Diet (LPD); and High Protein Diet (HPD). Plasma homocysteine [HCys] was measured to confirm consumption of dietary folic acid. Significantly, the FAS mice had decreased plasma HCys (p\u3c0.05). No significant differences were observed in physical activity across all 5 diets. As expected, CRP was stable, and a significant dietary effect for both folic acid and protein was observed with VEGF (p\u3c0.05). With Caspase-3, there was an emerging pattern of high FA and protein measured. Consumption of LPD did significantly decrease the ability to build a nest (p\u3c0.05), and, there was an emerging pattern with increased dietary protein intake that revealed more distance explored in the Open Field Test. Early data has demonstrated a link of diet and activity with chronic disease