Open Access
Subscription or Fee Access
Nutrigenomics and The Central Nervous System Disorders
Abstract
Aging is a dominant factor in Nutrigenomics and the central nervous system (CNS) disorders. Aging is a result of multifactorial processes and their interaction (environmental, heredity, and lifestyle). Human molecular approaches are motivated by way of physiological pathways in addition to exogenous factors, which consist of the weight loss program nutritional components that have substantial effects on metabolic health; as an example, bioactive molecules capable of selectively modulating metabolic pathways affect the progression of CNS disorders. As bioactive nutrients are increasingly recognized, their medical and molecular chemo preventive results are being characterized. Systematic analyses compassing the “omics” technology (transcriptomic, proteomics, and metabolomics) are being performed to discover their action. The evolving discipline of molecular pathological epidemiology has a unique power to analyze the consequences of nutritional and way of life publicity on scientific outcomes. The mounting body of understanding regarding food plan-related fitness status and sickness threat is anticipated to guide inside the near destiny to improve stepped forward diagnostic strategies and healing strategies focused on methods relevant to nutrients. The state of the art of aging and nutrigenomics studies and the molecular mechanisms underlying the beneficial effects of bioactive nutrients at the essential growing old-related problems arereviewed.
Keywords
References
National Research Council (U.S.) Committee on Population. Between Zeus and the Salmon;Wachter, K.W., Finch, C.E., Eds.; National Academies Press (U.S.): Washington, DC, USA, 1997.
Weinert, B.T.; Timiras, P.S. Invited review: Theories of aging. J. Appl. Physiol. 2003, 95, 1706–1716. [CrossRef][PubMed]
Yang, J.; Huang, T.; Song, W.; Petralia, F.; Mobbs, C.V.; Zhang, B.; Zhao, Y.; Schadt, E.E.; Zhu,J.; Tu, Z.Discover the network mechanisms underlying the connections between aging and age related diseases.Sci. Rep. 2016, 6, 32566. [CrossRef] [PubMed]
Srivastava, I.; Thukral, N.; Hasija, Y. Genetics of human age related disorders. Adv. Gerontol.Uspekhi Gerontol. 2015, 28, 228247.
Pizza, V.; Agresta, A.; D’Acunto, C.W.; Festa, M.; Capasso, A. Neuroinflammation and ageing:Current theories and an overview of the data. Rev. Recent Clin. Trials 2011, 6, 189–203. [CrossRef][PubMed]
Kowald, A.; Kirkwood, T.B. A network theory of ageing: The interactions of defective mitochondria, aberrant proteins, free radicals and scavengers in the ageing process. Mutat. Res.1996, 316, 209–236. [CrossRef]
Von Zglinicki, T.;Martin-Ruiz, C.M. Telomeres as biomarkers for ageing and age-related diseases.Curr.Mol.Med.2005, 5, 197–203. [CrossRef] [PubMed]
Bonfigli, A.R.; Spazzafumo, L.; Prattichizzo, F.; Bonafè, M.; Mensà, E.; Micolucci, L.; Giuliani,A.; Fabbietti, P.; Testa, R.; Boemi, M.; et al. Leukocyte telomere length and mortality risk in patients with type 2 diabetes. Oncotarget 2016, 7, 50835–50844. [CrossRef] [PubMed]
Olivieri, F.; Albertini, M.C.; Orciani, M.; Ceka, A.; Cricca, M.; Procopio, A.D.; Bonafè, M. DNA damage response (DDR) and senescence: Shuttled inflamma-miRNAs on the stage of inflamm aging. Oncotarget 2015, 6, 35509–35521. [PubMed]
Maslov, A.Y.; Vijg, J. Genome instability, cancer and aging. Biochim. Biophys. Acta Gen. Subj.2009, 1790,963–969. [CrossRef] [PubMed]
Dai, D.-F.; Chiao, Y.; Marcinek, D.J.; Szeto, H.H.; Rabinovitch, P.S. Mitochondrial oxidative stress in aging and healthspan. Longev. Health 2014, 3, 6. [CrossRef] [PubMed]
Bhatti, J.S.; Bhatti, G.K.; Reddy, P.H. Mitochondrial dysfunction and oxidative stress in metabolic disorders—A step towards mitochondria based therapeutic strategies. Biochim. Biophys. ActaMol.
Basis Dis.2016. [CrossRef] [PubMed]
Singhal, G.; Jaehne, E.J.; Corrigan, F.; Toben, C.; Baune, B.T. Inflammasomes in neuroinflammation and changes in brain function: A focused review. Front. Neurosci. 2014, 8, 315. [CrossRef] [PubMed]
Bessueille, L.; Magne, D. Inflammation: A culprit for vascular calcification in atherosclerosis and diabetes. Cell. Mol. Life Sci. 2015, 72, 2475–2489. [CrossRef] [PubMed]
Guarner, V.; Rubio-Ruiz, M.E. Low-grade systemic inflammation connects aging, metabolic syndrome and cardiovascular disease. Interdiscip. Top. Gerontol. 2015, 40, 99–106. [PubMed]
Franceschi, C.; Bonafè, M.; Valensin, S.; Olivieri, F.; de Luca, M.; Ottaviani, E.; de Benedictis, G.Inflamm-aging. An evolutionary perspective on immunosenescence. Ann. N. Y. Acad. Sci. 2000,908, 244–254. [CrossRef][PubMed]
De la Fuente, M.; Miquel, J. An update of the oxidation-inflammation theory of aging: The involvement of the immune system in oxi-inflamm-aging. Curr. Pharm. Des. 2009, 15, 3003–3026.
[CrossRef] [PubMed]
Ricordi, C.; Garcia-Contreras, M.; Farnetti, S. Diet and inflammation: Possible effects on immunity,chronic diseases, and life span. J. Am. Coll. Nutr. 2015, 34, 10–13. [CrossRef] [PubMed]
Pelicci, P.G.; Migliaccio, E.; Giorgio, M.; Mele, S.; Pelicci, G.; Reboldi, P.; Pandolfi, P.P.;Lanfrancone, L. The p66shc adaptor protein controls oxidative stress response and life span in mammals. Nature 1999, 402,309–313. [CrossRef] [PubMed]
Puca, A.A.; Daly, M.J.; Brewster, S.J.; Matise, T.C.; Barrett, J.; Shea-Drinkwater, M.; Kang, S.;Joyce, E.;Nicoli, J.; Benson, E.; et al. A genome-wide scan for linkage to human exceptional longevity identifies a locus on chromosome 4. Proc. Natl. Acad. Sci. USA 2001, 98, 10505–10508.[CrossRef] [PubMed]
Smith, R.G.; Betancourt, L.; Sun, Y. Molecular endocrinology and physiology of the aging central nervous system. Endocr. Rev. 2005, 26, 203–250. [CrossRef] [PubMed]
Pizza, V.; Agresta, A.; Iorio, E.L.; Capasso, A. Oxidative stress and aging: a clinical and biochemical study. Pharmacologyonline 2013, 2, 28–37.
Cannon,W.B. The Wisdom of the Body;W.W. Norton & Company: New York, NY, USA, 1932.
McEwen, B.S. The End of Stress as We Know It; Joseph Henry Press: Washington, DC,USA, 2002.
Selye, H. The Stress of Life; McGraw-Hill: New York, NY, USA, 1976
Nawata, H.; Yanase, T.; Goto, K.; Okabe, T.; Nomura, M.; Ashida, K.; Watanabe, T. Adrenopause.Horm. Res. 2004, 62, 110–114.[CrossRef] [PubMed]
Graham, D.;McLachlan, A. Decliningmelatonin levels and older people. How old is old? Neuro Endocrinol. Lett. 2004, 25, 415–418. [PubMed]
Arendt, J. Melatonin. Clin. Endocrinol. (Oxf.) 1988, 29, 205–229. [CrossRef] [PubMed]
Armstrong, S.M.; Redman, J.R. Melatonin: A chronobiotic with anti-aging properties? Med.Hypotheses 1991,34, 300–309. [CrossRef]
Bondy, S.C.; Sharman, E.H. Melatonin and the aging brain. Neurochem. Int. 2007, 50, 571–580.[CrossRef] [PubMed]
Pierpaoli,W.; Regelson,W. Pineal control of aging: Effect of melatonin and pineal grafting on aging mice. Proc. Natl. Acad. Sci. USA 1994, 91, 787–791. [CrossRef] [PubMed]
Karasek, M. Melatonin, human aging, and age-related diseases. Exp. Gerontol. 2004, 39, 1723–1729. [CrossRef][PubMed]
33 Rudman, D.; Feller, A.G.; Nagraj, H.S.; Gergans, G.A.; Lalitha, P.Y.; Goldberg, A.F.;Schlenker, R.A.; Cohn, L.; Rudman, I.W.; Mattson, D.E. Effects of human growth hormone in men over 60 years old. N. Engl. J. Med.1990, 323, 1–6. [CrossRef] [PubMed]
Nass, R.; Park, J.; Thorner, M.O. Growth hormone supplementation in the elderly. Endocrinol. Metab. Clin. N. Am. 2007, 36, 233–245. [CrossRef] [PubMed]
Snyder, P.J.; Peachey, H.; Hannoush, P.; Berlin, J.A.; Loh, L.; Lenrow, D.A.; Holmes, J.H.;Dlewati, A.; Santanna, J.; Rosen, C.J.; et al. Effect of testosterone treatment on body composition and muscle strength in men over 65 years of age. J. Clin. Endocrinol. Metab.1999, 84, 2647–2653.[CrossRef] [PubMed]
Stoll, B.A. Dietary supplements of dehydroepiandrosterone in relation to breast cancer risk. Eur. J. Clin. Nutr.1999, 53, 771–775. [CrossRef] [PubMed]
Effros, R.B. From Hayflick toWalford: The role of T cell replicative senescence in human aging. Exp. Gerontol. 2004, 39, 885–890. [CrossRef] [PubMed]
Zhang, H.; Puleston, D.J.; Simon, A.K. Autophagy and immune senescence. Trends Mol. Med.2016, 22, 671–686. [CrossRef][PubMed]
Franceschi, C. Cell proliferation, cell death and aging. Aging (Milano) 1989, 1, 3–15. [CrossRef][PubMed]
Franceschi, C.; Monti, D.; Sansoni, P.; Cossarizza, A. The immunology of exceptional individuals:The lesson of centenarians. Immunol. Today 1995, 16, 12–16. [CrossRef]
Franceschi, C.; Monti, D.; Barbieri, D.; Grassilli, E.; Troiano, L.; Salvioli, S.; Negro, P.; Capri, M.;Guido, M.; Azzi, R.; et al. Immunosenescence in Humans: Deterioration or Remodelling? Int. Rev.Immunol. 1995, 12,57–74. [CrossRef] [PubMed]
Hayflick, L. The limited in vitro lifetime of human diploid cell strains. Exp. Cell Res. 1965, 37,614–636.[CrossRef]
Judith, C. Cellular Senescence and Cell Death. In Physiological Basis of Aging and Geriatrics, 3rd ed.; Timiras, P.S., Ed.; CRC Press: Boca Raton, FL, USA, 2003; pp. 47–59.
Blackburn, E.H. Telomere states and cell fates. Nature 2000, 408, 53–56. [CrossRef] [PubMed]
Kim, N.W.; Piatyszek, M.A.; Prowse, K.R.; Harley, C.B.;West, M.D.; Ho, P.L.; Coviello,G.M.;Wright,W.E.; Weinrich, S.L.; Shay, J.W. Specific association of human telomerase activity with immortal cells and cancer. Science 1994, 266, 2011–2015. [CrossRef] [PubMed]
Reddel, R.R. The role of senescence and immortalization in carcinogenesis. Carcinogenesis 2000,21, 477–484.[CrossRef][PubMed]
Ferrara, N.; Corbi, G.; Scarpa, D.; Rengo, G.; Longobardi, G.; Mazzella, F.; Cacciatore, F.; Rengo,F. Teorie dell’invecchiamento The aging theories. G. Gerontol. 2005, 53, 57–74
l,Gerli, R.; Paganelli, R.; Cossarizza, A.; Muscat, C.; Piccolo, G.; Barbieri, D.; Mariotti, S.; Monti,D.; Bistoni, O.; Raiola, E.; et al. Long-term immunologic effects of thymectomy in patients with myasthenia gravis. J. Allergy Clin. Immunol. 1999, 103, 865–872. [CrossRef]
Effros, R.B. Ageing and the immune system. Novartis Found. Symp. 2001, 235, 146–149.
Fagnoni, F.F.; Vescovini, R.; Mazzola, M.; Bologna, G.; Nigro, E.; Lavagetto, G.; Franceschi, C.;Passeri, M.; Sansoni, P. Expansion of cytotoxic CD8+ CD28???? T cells in healthy ageing people,including centenarians. Immunology 1996, 88, 501–507. [CrossRef] [PubMed]
Timm, J.A.; Thoman, M.L. Maturation of CD4+ lymphocytes in the aged microenvironment results in a memory-enriched population. J. Immunol. 1999, 162, 711–717. [PubMed]
Effros, R.B. Long-term immunological memory against viruses. Mech. Ageing Dev. 2000, 121,161–171.[CrossRef]
Wikby, A.; Johansson, B.; Olsson, J.; Löfgren, S.; Nilsson, B.O.; Ferguson, F. Expansions of peripheral blood CD8 T-lymphocyte subpopulations and an association with cytomegalovirus seropositivity in the elderly: The Swedish NONA immune study. Exp. Gerontol. 2002, 37, 445–453. [CrossRef]
Pawelec, G.; Ouyang, Q.; Wagner, W.; Biol, D.; Wikby, A. Pathways to a robust immune response in the elderly. Immunol. Allergy Clin. N. Am. 2003, 23, 1–13. [CrossRef]
Bonafè, M.; Valensin, S.; Gianni, W.; Marigliano, V.; Franceschi, C. The unexpected contribution of immunosenescence to the leveling off of cancer incidence andmortality in the oldest old. Crit. Rev. Oncol. Hematol. 2001, 39, 227–233. [CrossRef]
Pahlavani, M.A. T cell signaling: Effect of age. Front. Biosci. 1998, 3, D1120–D1133. [CrossRef][PubMed]
Sansoni, P.; Cossarizza, A.; Brianti, V.; Fagnoni, F.; Snelli, G.; Monti, D.; Marcato, A.; Passeri, G.;Ortolani, C.; Forti, E. Lymphocyte subsets and natural killer cell activity in healthy old people and centenarians. Blood 1993, 82, 2767–2773. [PubMed]
Ogata, K.; Yokose, N.; Tamura, H.; An, E.; Nakamura, K.; Dan, K.; Nomura, T. Natural killer cells in the late decades of human life. Clin. Immunol. Immunopathol. 1997, 84, 269–275. [CrossRef]
[PubMed]
Remarque, E.; Pawelec, G. T-cell immunosenescence and its clinical relevance in man. Rev. Clin.Gerontol. 1998, 8, 5–14.[CrossRef]
Kourilsky, P.; Truffa-Bachi, P. Cytokine fields and the polarization of the immune response. Trends Immunol. 2001, 22, 502–509. [CrossRef]
Forsey, R.J.; Thompson, J.M.; Ernerudh, J.; Hurst, T.L.; Strindhall, J.; Johansson, B.; Nilsson, B.-O.; Wikby, A. Plasma cytokine profiles in elderly humans. Mech. Ageing Dev. 2003, 124, 487–493. [CrossRef]
Kerr, J.F.; Wyllie, A.H.; Currie, A.R. Apoptosis: A basic biological phenomenon with wide-ranging implications in tissue kinetics. Br. J. Cancer 1972, 26, 239–257. [CrossRef] [PubMed]
Akbar, A.N.; Salmon, M. Cellular environments and apoptosis: Tissue microenvironments control activated T-cell death. Immunol. Today 1997, 18, 72–76. [CrossRef]
Krammer, P.H. CD95’s deadly mission in the immune system. Nature 2000, 407, 789–795.[CrossRef] [PubMed]
Gupta, S. Molecular steps of death receptor and mitochondrial pathways of apoptosis. Life Sci.2001, 69, 2957–2964. [CrossRef]
Hengartner, M.O. The biochemistry of apoptosis. Nature 2000, 407, 770–776. [CrossRef][PubMed]
Jäättelä, M.; Tschopp, J. Caspase-independent cell death in T lymphocytes. Nat. Immunol. 2003, 4,416–423.[CrossRef] [PubMed]
Franceschi, C.; Valensin, S.; Bonafè, M.; Paolisso, G.; Yashin, A.I.; Monti, D.; De Benedictis, G.The network and the remodeling theories of aging: Historical background and new perspectives.Exp. Gerontol. 2000, 35, 879–896. [CrossRef]
De Martinis, M.; Franceschi, C.; Monti, D.; Ginaldi, L. Apoptosis remodeling in immunosenescence:Implications for strategies to delay ageing. Curr. Med. Chem. 2007, 14, 1389–1397. [CrossRef] [PubMed]
Franceschi, C.; Bonafè, M.; Valensin, S. Human immunosenescence: The prevailing of innate immunity, the failing of clonotypic immunity, and the filling of immunological space. Vaccine 2000, 18, 1717–1720.[CrossRef]
Finkel, T.; Holbrook, N.J. Oxidants, oxidative stress and the biology of ageing. Nature 2000, 408,239–247.[CrossRef] [PubMed]
Van Den Eeden, S.K.; Tanner, C.M.; Bernstein, A.L.; Fross, R.D.; Leimpeter, A.; Bloch, D.A.;Nelson, L.M. Incidence of Parkinson’s disease: Variation by age, gender, and race/ethnicity. Am. J. Epidemiol. 2003, 157, 1015–1022. [Google Scholar] [CrossRef] [PubMed]
De Lau, L.M.L.; Koudstaal, P.J.; Witteman, J.C.M.; Hofman, A.; Breteler, M.M.B. Dietary folate,vitamin B12, and vitamin B6 and the risk of Parkinson disease. Neurology 2006, 67, 315–318.[Google Scholar] [CrossRef]
74. Roy Sarkar, S.; Banerjee, S. Gut microbiota in neurodegenerative disorders. J. Neuroimmunol. 2019, 328, 98–104. [Google Scholar] [CrossRef] [PubMed]
Davies, K.J.A.; Sevanian, A.; Muakkassah-Kelly, S.F.; Hochstein,P. Uric acid-iron ion complexes. A new aspect of the antioxidant functions of uric acid. Biochem. J. 1986, 235, 747–754. [Google
Scholar] [CrossRef]
Crotty, G.F.; Ascherio, A.; Schwarzschild, M.A. Targeting urate to reduce oxidative stress in Parkinson disease. Exp. Neurol. 2017, 298, 210–224. [Google Scholar] [CrossRef]
Vitart, V.; Rudan, I.; Hayward, C.; Gray, N.K.; Floyd, J.; Palmer, C.N.A.; Knott, S.A.; Kolcic, I.; Polasek, O.; Graessler, J.; et al. SLC2A9 is a newly identified urate transporter influencing serum urate concentration, urate excretion and gout. Nat. Genet. 2008, 40, 437 442. [Google Scholar][CrossRef]
Church, W.H.; Ward, V.L. Uric acid is reduced in the substantia nigra in Parkinson’s disease: Effecton dopamine oxidation. Brain Res. Bull. 1994, 33, 419–425. [Google Scholar] [CrossRef]
Eriksson, A.-K.; Löfving, S.; Callaghan, R.C.; Allebeck, P. Alcohol use disorders and risk of Parkinson’s disease: Findings from a Swedish national cohort study 1972–2008. BMC Neurol. 2013, 13, 190. [Google Scholar] [CrossRef]
Sääksjärvi, K.; Knekt, P.; Männistö, S.; Lyytinen, J.; Jääskeläinen, T.; Kanerva, N.; Heliövaara, M. Reduced risk of Parkinson’s disease associated with lower body mass index and heavy leisure-time physical activity. Eur. J. Epidemiol. 2014, 29, 285–292. [Google Scholar] [CrossRef]
Noyce, A.J.; Bestwick, J.P.; Silveira-Moriyama, L.; Hawkes, C.H.; Giovannoni, G.; Lees, A.J.;Schrag, A. Meta-analysis of early nonmotor features and risk factors for Parkinson disease. Ann. Neurol. 2012, 72, 893–901. [Google Scholar] [CrossRef]
Alzheimer’s Association. 2014 Alzheimer’s disease facts and figures. Alzheimers Dement. 2014;10:e47–92. [PubMed] [Google Scholar]
Prince M, Wimo A, Guerchet M, Ali GC, Wu YT, Prina AM. World Alzheimer Report 2015: the global impact of dementia. London (UK): Alzheimer’s Disease International; 2015. [Google Scholar]
Do Carmo S, Cuello AC. Modeling Alzheimer’s disease in transgenic rats. Mol Neurodegener 2013;8:37. [PMC free article] [PubMed] [Google Scholar]
Shewale SJ, Huebinger RM, Allen MS, Barber RC. The potential role of epigenetics in Alzheimer’s disease etiology. Biol Syst 2013;2:114. [Google Scholar]
Chin-Chan M, Navarro-Yepes J, Quintanilla-Vega B. Environmental pollutants as risk factors for neurodegenerative disorders: Alzheimer and Parkinson diseases. Front Cell Neurosci 2015;9:124. [PMC free article] [PubMed] [Google Scholar]
Nicolia V, Lucarelli M, Fuso A. Environment, epigenetics and neurodegeneration: focus on nutrition in Alzheimer’s disease. Exp Gerontol 2015;68:8–12. [PubMed] [Google Scholar]
Wainaina MN, Chen Z, Zhong C. Environmental factors in the development and progression of late-onset Alzheimer’s disease. Neurosci Bull 2014;30:253–70. [PMC free article] [PubMed] [Google Scholar]
Tyler CR, Allan AM. The effects of arsenic exposure on neurological and cognitive dysfunction in human and rodent studies: a review. Curr Environ Health Rep 2014;1:132–47. [PMC free article] [PubMed] [Google Scholar]
Moore MR. Lead in drinking water in soft water areas—health hazards. Sci Total Environ 1977;7:109–15. [PubMed] [GoogleScholar]
Percy ME, Kruck TP, Pogue AI, Lukiw WJ. Towards the prevention of potential aluminum toxic effects and an effective treatment for Alzheimer’s disease. J Inorg Biochem 2011;105:1505–12. [PMC free article] [PubMed] [Google Scholar]
Maruszak A, Pilarski A, Murphy T, Branch N, Thuret S.Hippocampal neurogenesis in Alzheimer’s disease: is there a role for dietary modulation? J Alzheimers Dis 2014;38:11–38. [PubMed] [Google Scholar]
Marques S, Outeiro TF. Epigenetics in Parkinson’s and Alzheimer’s diseases. Subcell Biochem 2013;61:507–25. [PubMed] [Google Scholar]
GBD 2016 Epilepsy Collaborators. Global, regional, and national burden of epilepsy, 1990–2016:A systematic analysis for the Global Burden of Disease Study 2016. Lancet Neurol. 2019, 18, 357–375. [Google Scholar] [CrossRef]
Singh, A.; Trevick, S. The epidemiology of global epilepsy. Neurol. Clin. 2016, 34, 837–847.[Google Scholar] [CrossRef] [PubMed]
Ułamek-Kozioł, M.; Pluta, R.; Bogucka-Kocka, A.; Czuczwar, S.J. To treat or not to treat drug-refractory epilepsy by the ketogenic diet? That is the question. Ann. Agric. Environ. Med. 2016, 23,646–649. [Google Scholar] [CrossRef]
Zhang, Y.; Zhou, S.; Zhou, Y.; Yu, L.; Zhang, L.; Wang, Y. Altered gut microbiome composition in children with refractory epilepsy after ketogenic diet. Epilepsy Res. 2018, 145, 163–168. [Google Scholar] [CrossRef]
Lindefeldt, M.; Eng, A.; Darban, H.; Bjerkner, A.; Zetterström, C.K.; Allander, T.; Andersson, B.;Borenstein, E.; Dahlin, M.; Prast-Nielsen, S. The ketogenic diet influences taxonomic and functional composition of the gut microbiota in children with severe epilepsy. NPJ Biofilms Microb. 2019, 5, 5. [Google Scholar] [CrossRef]
Xie, G.; Zhou, Q.; Qiu, C.Z.; Dai, W.K.; Wang, H.P.; Li, Y.H.; Liao, J.X.; Lu, X.G.; Lin, S.F.; Ye, J.H.; et al. Ketogenic diet poses a significant effect on imbalanced gut microbiota in infants with refractory epilepsy. World J. Gastroenterol. 2017, 23, 6164–6171. [Google Scholar] [CrossRef]
Spinelli, E.; Blackford, R. Gut microbiota, the ketogenic diet and epilepsy. Pediatr. Neurol.Briefs. 2018, 32, 10. [Google Scholar] [CrossRef]
Refbacks
- There are currently no refbacks.