Green Tea Catechins as Neuroprotective Agents: Systematic Review of the Literature in Animal Pre-Clinical Trials
DOI:
https://doi.org/10.17140/aftnsoj-1-108Keywords:
Green Tea Catechins, EGCG, Oxidative stress, Neuroprotection, Pre-clinical animal trials, Alzheimer’s disease, Beta amyloids, Tau proteinAbstract
Alzheimer’s Disease (AD) is a neurodegenerative disorder and the most common form of dementia, with symptoms and manifestations that progressively get worse with increasing age. Therefore, with the ageing of the population worldwide, the prevalence of AD is increasing. There is no current cure for AD and, as a result, there has been a recent rise in interest in plant bioactive compounds that may prevent or improve symptoms of the disease. Currently, the nootropic potential of plant derived compounds that can combat damage posed by free radicals is being investigated. Antioxidants, in particular, the Green Tea Catechins (GTC), have been shown significant interest due to their exceptionally strong antioxidant and anti-inflammatory properties. The aim of this paper was to perform a systematic review based on the PRISMA guidelines in order to evaluate the effectiveness of GTC as a potential treatment to suppress or delay the onset of AD in pre-clinical animal trials. The paper reports on three animal pre-clinical trials in which rat or mice models of AD were used to test the effects of GTC or the pure form of the predominant GTC, Epigallocatechin gallate (EGCG), administered orally or by injection. The reviewed papers show that GTC extracts or pure EGCG had preventative effects on AD in the various animal models used, including the enhancement of learning and memory, possibly through the reduction in oxidative stress, β-amyloid plaque build up and Tau protein phosphorylation. Therefore, GTC extracts or EGCG in its pure form may serve as nootropic options in the prevention or treatment of neurodegeneration-associated diseases such as AD.
References
WHO. The World health report 2001-Mental Health: New Understanding, New Hope. Website: http://www.who.int/ whr/2001/en/. 2001; Accessed 2015
Collins PY, Patel V, Joestl SS, March D, Insel TR, Daar AS et al. Grand challenges in global mental health. Nature. 2011; 475(7354): 27-30. doi: 10.1038/475027a
Dixon J, Ferdinand M, D’Amico F, Knapp M. Exploring the cost-effectiveness of a one-off screen for dementia (for people aged 75 years in England and Wales). Int J Geriatr Psychiatry. 2015; 30(5): 446-452. doi: 10.1002/gps.4158
Giebel CM, Sutcliffe C, Challis D. Activities of daily living and quality of life across different stages of dementia: A UK study. Aging Ment Health. 2015; 19(1): 63-71. doi: 10.1080/13607863.2014.915920
Russ TC, Gatz M, Pedersen NL, et al. Geographical variation in dementia: examining the role of environmental factors in Sweden and Scotland. Epidemiology. 2015; 26(2): 263-270. doi: 10.1097/EDE.0000000000000230
Murray CJL, Lopez AD. A Comprehensive assessment of mortality and disability from diseases, injuries, and risk factors in 1990 and projected to 2020. Global Burden of Disease and Injury Series. 1996, Harvard School of Public Health on behalf of the World Health Organization and the World Bank. 43
APA. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Arlington, VA, USA: American Psychiatric Association; 2013
Pansari K, Gupta A, Thomas P. Alzheimer’s disease and vas-Open cular factors: Facts and theories. International Journal of Clinical Practice. 2002; 56(3): 197-203
Lopez OL, Kuller LH, Fitzpatrick A, Ives D, Becker JT, Beauchamp N. Evaluation of dementia in the cardiovascular health cognition study. Neuroepidemiology. 2003; 22(1): 1-12. doi: 10.1159/000067110
Holstein J, Chatellier G, Piette F, Moulias R. Prevalence of associated diseases in different types of dementia among elderly institutionalized patients: Analysis of 3447 records. J Am Geriatr Soc. 1994; 43(4): 972-977
Jackson GA, Dementia: Alzheimer’s disease. Nurs Times. 2002; 98(45): 32-34
Larson EB, Shadlen MF, Wang L, et al. Survival after initial diagnosis of Alzheimer disease. Ann Intern Med. 2004; 140(7): 501-509. doi: 10.7326/0003-4819-140-7-200404060-00008
Schwartz, S, Abnormal Psychology. Mauntain View. California, USA: Mayfield Publishing Company; 2000
McKeel DW Jr, Price JL, Miller JP, et al. Neuropathologic criteria for diagnosing Alzheimer disease in persons with pure dementia of Alzheimer type. J Neuropathol Exp Neurol. 2004; 63(10): 1028-1037
Zea-Sevilla MA, Fernández-Blázquez MA, Calero M, Bermejo-Velasco P, Rábano A. Combined Alzheimer and cerebrovascular staging explains advanced dementia cognition. Alzheimers Dement. 2015; pii: S1552-5260(15)00059-X.doi: 10.1016/j. jalz.2015.01.004
Kumar A, Singh A, Ekavali. A review on Alzheimer’s disease pathophysiology and its management: an update. Pharmacol Rep. 2015; 67(2): 195-203. doi: 10.1016/j.pharep.2014.09.004
Clark CM, Karlawish JH. Alzheimer disease: current concepts and emerging diagnostic and therapeutic strategies. Ann Intern Med. 2003; 138(5): 400-410. doi: 10.7326/0003-4819- 138-5-200303040-00010
Miller JW, Green R, Mungas DM, Reed BR, Jagust WJ. Homocysteine, vitamin B-6, and vascular disease in AD patients. Neurology. 2002; 58(10): 1471-1475
Zhu X, Raina AK, Lee HG, Casadesus G, Smith MA, Perry G. Oxidative stress signalling in Alzheimer’s disease. Brain Res. 2004; 1000(1-2): 32-39. doi: 10.1016/j.brainres.2004.01.012
Barnham KJ, Masters CL, Bush AI. Neurodegenerative diseases and oxidative stress. Nat Rev Drug Discov. 2004; 3(3): 205-214
Mace S, Cousin E, Ricard S, et al. ABCA2 is a strong genetic Journal risk factor for early-onset Alzheimer’s disease. Neurobiol Dis. 2005; 18(1): 119-125. doi: 10.1016/j.nbd.2004.09.011
Kan R, Wang B, Zhang C, et al. Genetic association of BACE1 gene polymorphism C786G with late-onset Alzheimer’s disease in chinese. J Mol Neurosci. 2005; 25(2): 127-132. doi: 10.1385/JMN:25:2:127
Zekanowski C, Styczyńska M, Pepłońska B, et al. Mutations in presenilin 1, presenilin 2 and amyloid precursor protein genes in patients with early-onset Alzheimer’s disease in Poland. Exp Neurol. 2003; 184(2): 991-996. doi: 10.1016/S0014-4886- (03)00384-4
Sobow T, Flirski M, Liberski PP. Amyloid-beta and tau proteins as biochemical markers of Alzheimer’s disease. Acta Neurobiol Exp (Wars). 2004; 64(1): 53-70
Kowalska A. The beta-amyloid cascade hypothesis: a sequence of events leading to neurodegeneration in Alzheimer’s disease. Neurol Neurochir Pol. 2004; 38(5): 405-411
Vauzour D, Vafeiadou K, Rodriguez-Mateos A, Rendeiro C, Spencer JP. The neuroprotective potential of flavonoids: a multiplicity of effects. Genes Nutr. 2008; 3(3-4): 115-126.. doi: 10.1007/s12263-008-0091-4
Vauzour D. Dietary polyphenols as modulators of brain functions: biological actions and molecular mechanisms underpinning their beneficial effects. Oxid Med Cell Longev; 2012. 2012: 914273. doi: 10.1155/2012/914273
Pavlica S, Gebhardt R. Protective effects of ellagic and chlorogenic acids against oxidative stress in PC12 cells. Free Radic Res. 2005; 39(12): 1377-1390. doi: 10.1080/09670260500197660
Wang Q, Sun AY, Simonyi A, et al. Neuroprotective mechanisms of curcumin against cerebral ischemia-induced neuronal apoptosis and behavioral deficits. J Neurosci Res. 2005; 82(1): 138-148. doi: 10.1002/jnr.20610
Borriello A, Cucciolla V, Della Ragione F, Galletti P. Dietary polyphenols: focus on resveratrol, a promising agent in the prevention of cardiovascular diseases and control of glucose homeostasis. Nutr Metab Cardiovasc Dis, 2010; 20(8): 618-625. doi: 10.1016/j.numecd.2010.07.004
Dai J, Mumper RJ. Plant phenolics: extraction, analysis and their antioxidant and anticancer properties. Molecules. 2010; 15(10): 7313-7352. doi: 10.3390/molecules15107313
Franz C, Chizzola R, Novak J, Sponza S. Botanical species being used for manufacturing plant food supplements (PFS) and related products in the EU member states and selected third countries. Food Funct. 2011; 2(12): 720-730. doi: 10.1039/ Open c1fo10130g
Recio MC, AndujarI, Rios JL. Anti-inflammatory agents from plants: progress and potential. Curr Med Chem. 2012; 19(14): 2088-2103. doi: 10.2174/092986712800229069
Schaffer S, Asseburg H, Kuntz S, Muller WE, Eckert GP. Effects of polyphenols on brain ageing and Alzheimer’s disease: focus on mitochondria. Mol Neurobiol. 2012; 46(1): 161-178. doi: 10.1007/s12035-012-8282-9
Lorrain, B, et al. Evolution of analysis of polyhenols from grapes, wines, and extracts. Molecules. 2013; 18(1): 1076-1100. doi: 10.3390/molecules18011076
Naumovski N. Bioactive Composition of Plants and Plant Foods, in Plant Bioactive Compounds for Pancreatic Cancer Prevention and Treatment. In Scarlett CJ, Vuong QV. Nova Publishers: New York. 2015; 322
Eschenauer G, Sweet BV. Pharmacology and therapeutic uses of theanine. Am J Health Syst Pharm. 2006. 63(1): 26, 28- 30. doi: 10.2146/ajhp050148
Vuong QV, Golding JB, Nguyen M, Roach PD. Extraction and isolation of catechins from tea. J Sep Sci. 2010; 33(21): 3415-3428. doi: 10.1002/jssc.201000438
Khan MA, Hussain A, Sundaram MK, et al. (-)-Epigallocatechin-3-gallate reverses the expression of various tumor-suppressor genes by inhibiting DNA methyltransferases and histone deacetylases in human cervical cancer cells. Oncol Rep. 2015; 33(4): 1976-1984. doi: 10.3892/or.2015.3802
Shan HM, Shi Y, Quan J. Identification of green tea catechins as potent inhibitors of the polo-box domain of polo-like kinase 1. ChemMedChem. 2015; 10(1): 158-163. doi: 10.1002/ cmdc.201402284
Nabavi SM, Daglia M, Moghaddam AH, Nabavi SF, Curti V. Tea consumption and risk of ischemic stroke: a brief review of the literature. Curr Pharm Biotechnol. 2014; 15(4): 298-303. doi: 10.2174/1389201015666140617100945
Li M, Hagerman AE. Role of the flavan-3-ol and galloyl moieties in the interaction of (-)-epigallocatechin gallate with serum albumin. J Agric Food Chem. 2014; 62(17): 3768-3775. doi: 10.1021/jf500246m
Koutelidakis AE, Rallidis L, Koniari K, et al. Effect of green tea on postprandial antioxidant capacity, serum lipids, C-reactive protein and glucose levels in patients with coronary artery disease. Eur J Nutr. 2014; 53(2): 479-486. doi: 10.1007/s00394- 013-0548-0
Hagiwara M, Matsushita K. Epigallocatechin gallate sup-Journal presses LPS endocytosis and nitric oxide production by reducing Rab5-caveolin-1 interaction. Biomed Res. 2014; 35(2): 145-151. doi: 10.2220/biomedres.35.145
Cai J, Jing D, Shi M, et al. Epigallocatechin gallate (EGCG) attenuates infrasound-induced neuronal impairment by inhibiting microglia-mediated inflammation. J Nutr Biochem. 2014; 25(7): 716-725. doi: 10.1016/j.jnutbio.2014.02.012
Yang EJ, Lee J, Lee SY, et al. EGCG attenuates autoimmune arthritis by inhibition of STAT3 and HIF-1alpha with Th17/Treg control. PLoS One. 2014; 9(2): e86062. doi: 10.1371/journal. pone.0086062
Liu D, Zhang X, Jiang L, Guo Y, Zheng C. Epigallocatechin- 3-gallate (EGCG) attenuates concanavalin A-induced hepatic injury in mice. Acta Histochem. 2014; 116(4): 654-662. doi: 10.1016/j.acthis.2013.12.002
Apetz N, Munch G, Govindaraghavan S, Gyengesi E. Natural compounds and plant extracts as therapeutics against chronic inflammation in Alzheimer’s disease--a translational perspective. CNS Neurol Disord Drug Targets. 2014; 13(7): 1175-1191. doi: 10.2174/1871527313666140917110635
Nguyen P, Derreumaux P. Understanding amyloid fibril nucleation and abeta oligomer/drug interactions from computer simulations. Acc Chem Res. 2014; 47(2): 603-611. doi: 10.1021/ ar4002075
Lee HS, Jun JH, Jung EH, Koo BA, Kim YS. Epigalloccatechin-3-gallate inhibits ocular neovascularization and vascular permeability in human retinal pigment epithelial and human retinal microvascular endothelial cells via suppression of MMP-9 and VEGF activation. Molecules. 2014; 19(8): 12150-12172. doi: 10.3390/molecules190812150
Betts JW, Wareham DW. In vitro activity of curcumin in combination with epigallocatechin gallate (EGCG) versus multidrug-resistant Acinetobacter baumannii. BMC Microbiol. 2014; 14: 172. doi: 10.1186/1471-2180-14-172
Zhao J, Suyama A, Tanaka M, Matsui T. Ferulic acid enhances the vasorelaxant effect of epigallocatechin gallate in tumor necrosis factor-alpha-induced inflammatory rat aorta. J Nutr Biochem. 2014; 25(7): 807-814. doi: 10.1016/j.jnutbio.2014.03.013
Reygaert WC. The antimicrobial possibilities of green tea. Front Microbiol. 2014; 5: 434. doi: 10.3389/fmicb.2014.00434
Gundimeda U, McNeill TH, Fan TK, et al. Green tea catechins potentiate the neuritogenic action of brain-derived neurotrophic factor: role of 67-kDa laminin receptor and hydrogen peroxide. Biochem Biophys Res Commun. 2014; 445(1): 218- 224. doi: 10.1016/j.bbrc.2014.01.166 Open
Saiko P, Steinmann MT, Schuster H, et al. Epigallocatechin gallate, ellagic acid, and rosmarinic acid perturb dNTP pools and inhibit de novo DNA synthesis and proliferation of human HL-60 promyelocytic leukemia cells: Synergism with arabinofuranosylcytosine. Phytomedicine. 2015; 22(1): 213-222. doi: 10.1016/j.phymed.2014.11.017
Wei R, Zhu G, Jia N, Yang W. Epigallocatechin-3-gallate sensitizes human 786-O renal cell carcinoma cells to TRAILinduced apoptosis. Cell Biochem Biophys. 2014. doi: 10.1007/ s12013-014-0428-0
Eom DW, Lee JH, Kim YJ, et al. Synergistic effect of curcumin on epigallocatechin gallate-induced anticancer action in PC3 prostate cancer cells. BMB Rep. 2014; pii: 2990
Moher D, Liberati A, Tetzlaff J, Altman DG; PRISMA Group. Preferred reporting items for systematic reviews and meta-analyses: The PRISMA statement. Int J Surg. 2010; 8(5): 336-341. doi: 10.7326/0003-4819-151-4-200908180-00135
Haque AM, Hashimoto M, Katakura M, Hara Y, Shido O. Green tea catechins prevent cognitive deficits caused by Abeta1- 40 in rats. J Nutr Biochem. 2008; 19(9): 619-626. doi: 10.1016/j. jnutbio.2007.08.008
Levites Y, Weinreb O, Maor G, Youdim MB, Mandel S. Green tea polyphenol (-)-epigallocatechin-3-gallate prevents Nmethyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced dopaminergic neurodegeneration. J Neurochem. 2001; 78(5): 1073-1082. doi: 10.1046/j.1471-4159.2001.00490.x
Rezai-Zadeh K, Arendash GW, Hou H, et al. Green tea epigallocatechin-3-gallate (EGCG) reduces beta-amyloid mediated cognitive impairment and modulates tau pathology in Alzheimer transgenic mice. Brain Res. 2008; 1214: 177-187. doi: 10.1016/j. brainres.2008.02.107
Saeed NM, El-Naga RN, El-Bakly WM, Abdel-Rahman HM, El-Demerdash E. Epigallocatechin-3-gallate pretreatment attenuates doxorubicin-induced cardiotoxicity in rats: A mechanistic study. Biochem Pharmacol. 2015; pii: S0006-2952- (15)00110-0. doi: 10.1016/j.bcp.2015.02.006
Joshi R, Rana A, Gulati A. Studies on quality of orthodox teas made from anthocyanin-rich tea clones growing in Kangra valley, India. Food Chem. 2015; 176: 357-366. doi: 10.1016/j. foodchem.2014.12.067
Obregon DF, Rezai-Zadeh K, Bai Y, et al. ADAM10 activation is required for green tea (-)-epigallocatechin-3-gallateinduced alpha-secretase cleavage of amyloid precursor protein. J Biol Chem. 2006; 281(24): 16419-16427. doi: 10.1074/jbc. M600617200 Journal
Lichtenthaler SF, Haass C. Amyloid at the cutting edge: Activation of alpha-secretase prevents amyloidogenesis in an Alzheimer disease mouse model. J Clin Invest. 2004; 113(10): 1384-1387. doi: 10.1172/JCI21746
Dickey CA, Kamal A, Lundgren K, et al. The high-affinity HSP90-CHIP complex recognizes and selectively degrades phosphorylated tau client proteins. J Clin Invest. 2007; 117(3): 648-658. doi: 10.1172/JCI29715
Kosik KS, Shimura H. Phosphorylated tau and the neurodegenerative foldopathies. Biochim Biophys Acta. 2005; 1739(2-3): 298-310. doi: 10.1016/j.bbadis.2004.10.011
Khan SG, Katiyar SK, Agarwal R, Mukhtar H. Enhancement of antioxidant and phase II enzymes by oral feeding of green tea polyphenols in drinking water to SKH-1 hairless mice: Possible role in cancer chemoprevention. Cancer Res. 1992; 52(14): 4050-4052
McGahon BM, Martin DS, Horrobin DF, Lynch MA. Agerelated changes in LTP and antioxidant defenses are reversed by an alpha-lipoic acid-enriched diet. Neurobiol Aging. 1999; 20(6): 655-664. doi: 10.1016/S0197-4580(99)00050-0
Murray CA, Lynch MA. Dietary supplementation with vitamin E reverses the age-related deficit in long term potentiation in dentate gyrus. J Biol Chem. 1998; 273(20): 12161-12168. doi: 10.1074/jbc.273.20.12161
Published
How to Cite
Issue
Section
License

This work is licensed under a Creative Commons Attribution 4.0 International License.
All content published in Advances in Food Technology and Nutrition Sciences (AFTNS) is licensed under the Creative Commons Attribution 4.0 International License (CC BY 4.0). This license allows anyone to copy, distribute, transmit, and adapt the work — including for commercial purposes — provided appropriate credit is given to the original author(s) and source.