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American Journal of Medical and Biological Research. 2017, 5(1), 1-8
DOI: 10.12691/AJMBR-5-1-1
Review Article

The Role of Nutritional Status in Neuroepigenetic Modification

Francis Gregory Samonte1,

1University of the Philippines Manila, Philippines

Pub. Date: May 25, 2017
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Cite this paper

Francis Gregory Samonte. The Role of Nutritional Status in Neuroepigenetic Modification. American Journal of Medical and Biological Research. 2017; 5(1):1-8. doi: 10.12691/AJMBR-5-1-1

Abstract

The study of epigenetic has brought about a deeper understanding of developmental programming through a complex network of modifications involving the DNA. While the DNA sequence remains conservative throughout, the mechanism of epigenetic modification involves changes through histone modification, DNA methylation, and chromatin remodeling. The overall dynamic effect of epigenetic modification allows the gene expression to be altered leading to a diverse phenotypical expression; a functional change in the genome without affecting the DNA. The emergence of nutritional neuroepigenetic serves to bring into focus the impact of nutrition as an environmental agent in regulating gene expression patterns leading to phenotypical expression with profound neurological and cognitive implication in later life. This link is supported by evidence from animal models suggesting that epigenetic marks, which are formed following DNA methylation or histone modification, can induce changes leading to developmental diseases or persist into adulthood. The difficulty in understanding the intrinsic biomolecular correlation between 1) epigenetic modification, 2) nutritional imbalance, and 3) cognitive impairment in an animal based model provides a compelling question regarding the developmental origins of cognitive related diseases. There have been few animal model studies involving the molecular basis of neuroepigenetic dysfunction in the relation to overnutrition or under nutrition. The main criteria in this review will focus on the few animal based studies in nutrition based epigenetic reprogramming and its role in neuroepigenetic dysregulation and cognitive impairment.

Keywords

cognition, autism, dementia, malnutrition, obesity, neuroepigenetic, memory

Copyright

Creative CommonsThis work is licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

References

[1]  Choi, SW., & and Friso, S. (2010). Epigenetics: A New Bridge between Nutrition and Health. American Society for Nutrition, 1, 8-16.
 
[2]  Perera, F., Herbstman, J. (2011). Prenatal environmental exposures, epigenetics and diseases. Reproductive Toxicology, 31(3), 363-373.
 
[3]  Pogribny, I., Karpf, A., James, S., et al. (2008). Epigenetic alterations in the brains of fisher 344 rats induced by long-term administration of folate/ methyl-deficient diet. Brain Research, 1237, 25-34.
 
[4]  Radford, EJ., Ito, M., Shi, H., et al. (2014). In utero undernourishment perturbs the adult sperm methylome and is linked to metabolic disease transmission. Science. 2014; 345(6198): 1255903.
 
[5]  Weksberg, R., Smith, AC.. (2003). Beckwith-Wiedemann syndrome demonstrates a role for epigenetic control of normal development. Human Molecular Genetics. 1, 12 Spec No 1: R61-8.
 
[6]  Tammen, SA., Friso, S., Choi, SW. (2013). Epigenetics: the link between nature and nurture. Molecular Aspects of Medicine, 34(4): 753-764.
 
[7]  Crider, KS., Yang, TP., Berry, RJ. (2012). Folate and DNA Methylation: A Review of Molecular Mechanisms and the Evidence for Folate’s Role. Advances in Nutrition, 3: 21-38.
 
[8]  Margueron, R., Reinberg, D. (2010). Chromatin Structure and the Inheritance of Epigenetic Information. Nature Reviews Genetics, 11, 285-296.
 
[9]  Vickers, MH. (2014). Early Life Nutrition, Epigenetics and Programming of Later Life Disease. Nutrients, 6, 2165-2178.
 
[10]  Dauncey, MJ. (2014). Nutrition, the brain and cognitive decline: insights from epigenetics. European Journal of Clinical Nutrition, 68(11):1179-85.
 
[11]  Handy, DE., Castro, R, Loscalzo, J. (2011). Epigenetic Modifications: Basic Mechanisms and Role in Cardiovascular Disease. Circulation, 123(19): 2145-2156.
 
[12]  Ruthenburg, AJ., Li, H., Patel, DJ., Allis CD. (2007). Multivalent engagement of chromatin modifications by linked binding modules. Nature Reviews Molecular Cell Biology, 8(12): 983-94.
 
[13]  Wang, Z., Zang, C., Rosenfeld, JA., et al. (2008). Combinatorial patterns of histone acetylations and methylations in the human genome. Nature Genetics, 40(7):897-903.
 
[14]  Krivtsov, AV., Feng Z., Lemieux, ME., et al. (2008). H3K79 methylation profiles define murine and human MLL-AF4 leukemias. Cancer Cell, 14(5): 355-68.
 
[15]  Guenther, MG., Levine SS., et al. (2007). A chromatin landmark and transcription initiation at most promoters in human cells. Cell, 130(1):77-88.
 
[16]  The AACR Human Epigenome Task Force & EUNE. (2008). Scientific Advisory Board, Nature, 454, 711-15.
 
[17]  Feinberg, AP., Tycko B. (2004). The history of cancer epigenetics. Nature Reviews Cancer, 4(2):143-53.
 
[18]  Dashwood RH. & Ho, E. (2007). Dietary histone deacetylase inhibitors: from cells to mice to man. Seminars in Cancer Biology, 17(5), 363-369.
 
[19]  Bassett, SA., Barnett, MPG. (2014). The Role of Dietary Histone Deacetylases (HDACs) Inhibitors in Health and Disease. Nutrients, 6(10): 4273-4301.
 
[20]  Volmar, CH. & Wahlestedt, C. (2015). Histone deacetylases (HDACs) and brain function. Neuroepigenetics, 1, 20-27.
 
[21]  Sun, H., Kennedy, PJ., Nestler, EJ. (2013). Epigenetics of the Depressed Brain: Role of Histone Acetylation and Methylation. Neuropsychopharmacology, 38(1):124-137.
 
[22]  Gold, PW. & Chrousos, GP. (2002). Organization of the stress system and its dysregulation in melancholic and atypical depression: high vs low CRH/NE states. Molecular Psychiatry, 7(3): 254-275.
 
[23]  Cavanaugh, SE., Pippin, JJ., Barnard, N. (2014). Animal Models of Alzheimer Disease: Historical Pitfalls and a Path Forward. Altex, 31(3):279-302.
 
[24]  Andrea Gawrylewsk. (2007). The Trouble with Animal Models. The Scientist, Volume 21(7).
 
[25]  Ge, ZJ., Luo, SM., Lin, F., et al. (2014). DNA methylation in oocytes and liver of female mice and their offspring: effects of high-fat-diet–induced obesity. Environmental Health Perspective, 122:159-164.
 
[26]  Kim, AY., Park, YJ., Pan, X., et al. (2015). Obesity-induced DNA hypermethylation of the adiponectin gene mediates insulin resistance. Nature Communications, 6: 7585.
 
[27]  Zhang, N. (2015). Epigenetic modulation of DNA methylation by nutrition and its mechanisms in animals. Animal Nutrition, 1(3): 144-151.
 
[28]  Zhang, P., Chu, T., Dedousis, N., et al. (2017). DNA methylation alters transcriptional rates of differentially expressed genes and contributes to pathophysiology in mice fed a high fat diet. Molecular Metabolism, 1-13.
 
[29]  Sharma, S., Taliyan, R. (2016). Epigenetic modifications by inhibiting histone deacetylases reverse memory impairment in insulin resistance induced cognitive deficit in mice. Neuropharmacology, 105: 285-97.
 
[30]  Barchuk, AR., Cristino, AS., Kucharski, R., et al. (2007). Molecular determinants of caste differentiation in the highly eusocial honeybee Apismellifera. BMC Developmental Biology, 7(70).
 
[31]  Evans, JD., Wheeler, DE. (1999). Differential gene expression between developing queens and workers in the honey bee, Apismellifera. Proceedings National Academy Science USA, 96(10): 5575-80.
 
[32]  Kucharski, R., Maleszka, J., et al. (2008). Nutritional control of reproductive status in honeybees via DNA methylation. Science, 319(5871): 1827-30.
 
[33]  Kangaspeska, S., Stride, B., Metivier, R., et al. (2008). Transient cyclical methylation of promoter DNA. Nature 452, 112-115.
 
[34]  Courtney, A., Miller, J., Sweatt, D. (2007). Covalent Modification of DNA Regulates Memory Formation. Neuron, 53(6), 857-869.
 
[35]  Métivier, R., Gallais, R., Tiffoche, C., et al. (2010). Cyclical DNA methylation of a transcriptionally active promoter. Nature, 463(7279): 384.
 
[36]  Miller, CA., Campbell, SL., Sweatt, JD. (2008). DNA methylation and histone acetylation work in concert to regulate memory formation and synaptic plasticity. Neurobiology of Learning and Memory, 89, 599-603.
 
[37]  Lubin, FD., Roth, TL., Sweatt, JD., (2008). Epigenetic regulation of BDNF gene transcription in the consolidation of fear memory. Journal of Neuroscience, 28, 10576-10586.
 
[38]  Brunaud, Alberto, Ayav, et al. (2003). Effects of vitamin B12 and folate deficiencies on DNA methylation and carcinogenesis in rat liver. Clinical Chemistry and Laboratory Medicine, 41(8):1012-9.
 
[39]  Chen, X., Hui, L., Geiger, JD. (2014). Role of LDL cholesterol and endolysosomes in amyloidogenesis and Alzheimer’s disease. Journal of Neurology & Neurophysiology, 5(5):236.
 
[40]  Fiorenza, MT., Dardis, A., Canterini, S., Erickson, RP. (2013). Cholesterol metabolism-associated molecules in late onset Alzheimer's disease. Journal of Biological Regulators & Homeostatic Agents, 27(2 Suppl): 23-35.
 
[41]  Milte, Parletta, Buckley, et al. (2012). Eicosapentaenoic and docosahexaenoic acids, cognition, and behavior in children with attention-deficit/hyperactivity disorder: a randomized controlled trial. Nutrition, 28(6): 670-7.
 
[42]  Bélanger, SA., Vanasse, M., Spahis, S., et al. (2009). Omega-3 fatty acid treatment of children with attention-deficit hyperactivity disorder: A randomized, double-blind, placebo-controlled study. Paediatrics & Child Health, 14(2):89-98.
 
[43]  Bryan, J., Traynor, AE. (2015). Renton Exploring the Epigenetics of Alzheimer Disease, JAMA Neurology, 72(1): 8-9.
 
[44]  Heyward FD., Gilliam D., Coleman MA., et al. (2016). Obesity Weighs down Memory through a Mechanism Involving the Neuroepigenetic Dysregulation of Sirt1. The Journal of Neuroscience 36(4): 1324-1335.
 
[45]  Varghese M., Wang J., Cheng A., et al. (2012). Epigenetic modification in metabolic syndrome-induced brain energy impairment. Alzheimer's & Dementia: The Journal of the Alzheimer's Association 8:4, 253-55.
 
[46]  Wang J., Freire D., Knable L., et al. (2015) Childhood and adolescent obesity and long-term cognitive consequences during aging. Journal of Comparative Neurology 523:5, 757-768.
 
[47]  Vucetic Z., Carlin JL., Totoki K., Reyes TM. (2012). Epigenetic dysregulation of the dopamine system in diet-induced obesity. J Neurochem. 120(6): 891-8.
 
[48]  Vucetic Z., Kimmel J., Reyes TM. (2011). Chronic High-Fat Diet Drives Postnatal Epigenetic Regulation of μ-Opioid Receptor in the Brain. Neuropsychopharmacology. 36(6): 1199-1206.
 
[49]  Hoek, HW., Brown, AS., Susser, E. (1998). The Dutch famine and schizophrenia spectrum disorders. Social Psychiatry and Psychiatric Epidemiology, 33(8): 373-9.
 
[50]  Liu, J., Zhao, SR., Reyes, T. (2015). Neurological and Epigenetic Implications of Nutritional Deficiencies on Psychopathology: Conceptualization and Review of Evidence. International Journal of Molecular Sciences, 16(8): 18129-18148.
 
[51]  Galler, JR., Bryce, CP., Zichlin, ML., et al. (2012). Infant Malnutrition Is Associated with Persisting Attention Deficits in Middle Adulthood. The Journal of Nutrition,142(4): 788-794.
 
[52]  Schmidt, AT., Alvarez, GC., Grove, WM., et al. (2012). Early iron deficiency enhances stimulus-response learning of adult rats in the context of competing spatial information. Developmental Cognitive Neuroscience, 2(1): 174-80.
 
[53]  Penido, AB., Rezende, GH., Abreu, RV., et al. (2012). Malnutrition during central nervous system growth and development impairs permanently the subcortical auditory pathway. Nutritional Neuroscience, 15(1): 31-6.
 
[54]  Rocinholi, LF., de Oliveira, LM., Colafêmina, JF. (2001). Malnutrition and environmental stimulation in rats: wave latencies of the brainstem auditory evoked potentials. Nutritional Neuroscience, 4(3): 199-212.
 
[55]  Udagawa J., Hino K. (2016). Impact of Maternal Stress in Pregnancy on Brain Function of the Offspring. Nihon Eiseigaku Zasshi 71(3):188-194.
 
[56]  Fuso A., Seminara L., Cavallaro RA., et al. (2005). S-adenosylmethionine/homocysteine cycle alterations modify DNA methylation status with consequent deregulation of PS1 and BACE and beta-amyloid production. Molecular and Cellular Neurosciences 28(1): 195-204.
 
[57]  Kronenberg G., Colla M., Endres M. (2009). Folic acid, neurodegenerative and neuropsychiatric disease. Current Molecular Medicine 9(3): 315-23.
 
[58]  Blegen, MB., Kennedy, BC., Thibert, KA., et al. (2013). Multigenerational effects of fetal-neonatal iron deficiency on hippocampal BDNF signaling. Physiological Reports, 1(5):e00096.
 
[59]  Schmidt, AT., Alvarez, GC., Grove, WM., et al. (2012). Early iron deficiency enhances stimulus-response learning of adult rats in the context of competing spatial information. Developmental Cognitive Neuroscience, 2(1): 174-80.
 
[60]  Hagmeyer, S., Haderspeck, JC., Grabrucker, AM. (2014). Behavioral impairments in animal models for zinc deficiency. Frontiers in Behavioral Neuroscience, 8: 443.
 
[61]  Sadli, N., Ackland, ML., De Mel, D., et al. (2012). Effects of zinc and DHA on the epigenetic regulation of human neuronal cells. Cellular Physiology & Biochemistry, 29(1-2): 87-98.