The Effects of Dietary Nitrate Supplementation as an Ergogenic Aid on NCAA Division Female Soccer Players

Undergraduate Researc

Examining a Relationship Between Chronic Dietary Folic Acid Deficiency and Activation of p53 Gene in Down Syndrome Ts65Dn Mice

Seaver Undergraduate Researc

DEFICIENT DIETARY FOLIC ACID AND SYSTEMIC DSP-4 INDUCED LOCUS COERULEUS LOSS ASSESSED AS NEURODEGENERATIVE COGNITIVE MODEL IN ADULT CB57/J6 MICE

DEFICIENT DIETARY FOLIC ACID AND SYSTEMIC DSP-4 INDUCED LOCUS COERULEUS LOSS ASSESSED AS NEURODEGENERATIVE COGNITIVE MODEL IN ADULT CB57/J6 MICE Gabriel Kong, C. Foster Graf, Aristotle Zeng, Theodore Helm, Simon Khorani, Rohan Rample, Smayana Kurapati, Riva Rainier, Aidan Schmidt, Maximilian Doane, David B. Green, and Susan E. Helm Chemistry and Nutritional Science, Pepperdine University, Malibu, California Dietary deficiency of folic acid (FA) shortened nerve lengths as much as 50% in hippocampal dentate gyrus (DG). Locus coeruleus (LC) is largest noradrenergic nucleus in central nervous system with neurogenic projections widely dispersed in the brain and, notably, a major norepinephrine source in the DG and frontal cortex (FC). For 16 weeks, adult CB57/J6 mice (N=66) were provided 4 dietary/DSP-4 treatments: NFCS (n=16, normal FA control, saline injected [0.2 mg FA/kg BW]); NFCD (n=18, normal FA, DSP-4 injected (50 mg DSP-4/kg BW); FADS (n=16, FA deficient, saline injected); and, FADD (n=16, FA deficient, DSP-4 injected). NE in FC was measured in addition to significant loss of LC neurons; astrocytes, calcium signaling, and embryonic neurons using, respectively, immunohistochemical methods for tyrosine hydroxylase (TH), GABA fibrillary acidic protein (GFAP), parvalbumin (PV), doublecortin (DCX) were analyzed. Confirmation of phenotypic cognitive behavior with Nesting Behavior; decreased distance traveled with Novel Object Recognition (NOR); and, decreased rearing and latency to explore to the center of the field in Open Field Testing (OFT) were enumerated between NFCS and FADD (

Examining the Role of Folic Acid Relative to Anxiety and Cognition in Mice

Roughly one-third of the population suffers from anxiety or neurocognitive disorders (Down Syndrome, Alzheimer’s) in their lifetime. However, whether folic acid deficiency causes anxiety or cognitive dysfunction remains relatively unexamined. The present study aims to explore the effects of folic acid deficiency and folic acid supplementation on cognitive function, memory, and anxiety-related behavior in mice. Sixteen-week-old C57BL/6J mice were fed a folic acid supplemented diet, a folic acid deficient diet, a high protein diet, a low protein diet, or a folate protein control diet for 8 weeks. A random representative sample of mice (N=38; 6-8 mice per dietary treatment) were tested. Three common methods utilized to examine states of anxiety and neurocognition are the following: 1) an Open Field Test to examine anxiety-related behavior and exploratory behavior; 2) a Novel Object Recognition test to assess memory and cognitive function; and, 3) Nestlet building, the ability to create a nest in 12 hours was conducted to assess hippocampal function. Consumption of a low protein diet did significantly decrease the ability to build a nest (p\u3c0.05), a result published with Down Syndrome mice. And, there was an emerging pattern with increased dietary protein intake that revealed more distance explored in the Open Field Test. Indeed, neurocognition was influenced at varying protein intake levels in our mice

Influence of Dietary Folic Acid on Methylenetetrahydrofolate Reductase (MTHFR) as a Biomarker of Down Syndrome in the Ts65Dn Mouse Model: Phases 1 and 2

The relationship between folic acid and Down Syndrome (DS) is one that demands further inquiry to establish a diet and genetic interaction. In this multiphase study, we are examining cognitive, behavioral and biochemical signs of dietary changes of folic acid in the DS mouse model. In Phase 1, 20 non-genetic mice were cared for over 10 weeks; half of the mice were fed a folic acid deficient diet. In Phase 2, 20 mice, (10 DS mice and 10 non-genetic mice) were cared for until the age of 4.5 months; all mice were fed a diet with adequate folic acid. At 10 and 14 weeks, nestlet tests were administered. Blood samples were collected and an assay was run to measure Methylenetetrahydrofolate Reductase (MTHFR). In Phases 1 and 2 of this project, the physiological stability of non-genetic mouse models with dietary changes, the baseline behavioral and cognitive activity of the DS mouse model, and the baseline biochemical measurements of MTHFR were established. Phase 1 (summer 2014) established that, with a deficiency of folic acid in the diet, the mice continue to gain weight steadily and fragility of the mouse model does not increase. In Phase 2 (fall 2014), it was established that there was a behavioral difference between the DS mouse model and the non-genetic mouse as measured by nestlet testing (p=0.000). Additionally, Phase 2 established that there was no statistical significance between the DS mouse model and the non-genetic mouse model (p=0.8). This verified that when fed the same diet, there is no difference in MTHFR activity in the DS mouse model and the non-genetic mouse. Phase 1 and Phase 2 results have contributed to the development of our Phase 3 dietary intervention with high and low folic acid and the changes in MTHFR

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

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