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      Association of Tea Consumption with Risk of Alzheimer’s Disease and Anti-Beta-Amyloid Effects of Tea

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          Abstract

          Neurodegenerative disease Alzheimer’s disease (AD) is attracting growing concern because of an increasing patient population among the elderly. Tea consumption is considered a natural complementary therapy for neurodegenerative diseases. In this paper, epidemiological studies on the association between tea consumption and the reduced risk of AD are reviewed and the anti-amyloid effects of related bioactivities in tea are summarized. Future challenges regarding the role of tea in preventing AD are also discussed.

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          Green tea epigallocatechin-3-gallate (EGCG) modulates amyloid precursor protein cleavage and reduces cerebral amyloidosis in Alzheimer transgenic mice.

          Jin Zeng, Terrence Town, Takashi Mori … (2005)
          Alzheimer's disease (AD) is a progressive neurodegenerative disorder pathologically characterized by deposition of beta-amyloid (Abeta) peptides as senile plaques in the brain. Recent studies suggest that green tea flavonoids may be used for the prevention and treatment of a variety of neurodegenerative diseases. Here, we report that (-)-epigallocatechin-3-gallate (EGCG), the main polyphenolic constituent of green tea, reduces Abeta generation in both murine neuron-like cells (N2a) transfected with the human "Swedish" mutant amyloid precursor protein (APP) and in primary neurons derived from Swedish mutant APP-overexpressing mice (Tg APPsw line 2576). In concert with these observations, we find that EGCG markedly promotes cleavage of the alpha-C-terminal fragment of APP and elevates the N-terminal APP cleavage product, soluble APP-alpha. These cleavage events are associated with elevated alpha-secretase activity and enhanced hydrolysis of tumor necrosis factor alpha-converting enzyme, a primary candidate alpha-secretase. As a validation of these findings in vivo, we treated Tg APPsw transgenic mice overproducing Abeta with EGCG and found decreased Abeta levels and plaques associated with promotion of the nonamyloidogenic alpha-secretase proteolytic pathway. These data raise the possibility that EGCG dietary supplementation may provide effective prophylaxis for AD.
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            Potent anti-amyloidogenic and fibril-destabilizing effects of polyphenols in vitro: implications for the prevention and therapeutics of Alzheimer's disease.

            Kenjiro Ono, Yuji Yoshiike, Akihiko Takashima … (2003)
            Cerebral deposition of amyloid beta-peptide (Abeta) in the brain is an invariant feature of Alzheimer's disease (AD). A consistent protective effect of wine consumption on AD has been documented by epidemiological studies. In the present study, we used fluorescence spectroscopy with thioflavin T and electron microscopy to examine the effects of wine-related polyphenols (myricetin, morin, quercetin, kaempferol (+)-catechin and (-)-epicatechin) on the formation, extension, and destabilization of beta-amyloid fibrils (fAbeta) at pH 7.5 at 37 degrees C in vitro. All examined polyphenols dose-dependently inhibited formation of fAbeta from fresh Abeta(1-40) and Abeta(1-42), as well as their extension. Moreover, these polyphenols dose-dependently destabilized preformed fAbetas. The overall activity of the molecules examined was in the order of: myricetin = morin = quercetin > kaempferol > (+)-catechin = (-)-epicatechin. The effective concentrations (EC50) of myricetin, morin and quercetin for the formation, extension and destabilization of fAbetas were in the order of 0.1-1 micro m. In cell culture experiments, myricetin-treated fAbeta were suggested to be less toxic than intact fAbeta, as demonstrated by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assay. Although the mechanisms by which these polyphenols inhibit fAbeta formation from Abeta, and destabilize pre-formed fAbetain vitro are still unclear, polyphenols could be a key molecule for the development of preventives and therapeutics for AD.
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              Green tea consumption and cognitive function: a cross-sectional study from the Tsurugaya Project 1.

              Shinichi Kuriyama, Atsushi Hozawa, Kaori Ohmori … (2006)
              Although considerable experimental and animal evidence shows that green tea may possess potent activities of neuroprotection, neurorescue, and amyloid precursor protein processing that may lead to cognitive enhancement, no human data are available. The objective was to examine the association between green tea consumption and cognitive function in humans. We analyzed cross-sectional data from a community-based Comprehensive Geriatric Assessment (CGA) conducted in 2002. The subjects were 1003 Japanese subjects aged > or =70 y. They completed a self-administered questionnaire that included questions about the frequency of green tea consumption. We evaluated cognitive function by using the Mini-Mental State Examination with cutoffs of or =2 cups/d (P for trend = 0.0006). Corresponding ORs were 1.00 (reference), 0.60 (95% CI: 0.35, 1.02), and 0.87 (95% CI: 0.55, 1.38) (P for trend = 0.33) for black or oolong tea and 1.00 (reference), 1.16 (95% CI: 0.78, 1.73), and 1.03 (95% CI: 0.59, 1.80) (P for trend = 0.70) for coffee. The results were essentially the same at cutoffs of <28 and <24. A higher consumption of green tea is associated with a lower prevalence of cognitive impairment in humans.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Nutrients
                Journal ID (iso-abbrev): Nutrients
                Journal ID (publisher-id): nutrients
                Title: Nutrients
                Publisher: MDPI
                ISSN (Electronic): 2072-6643
                Publication date (Electronic): 22 May 2018
                Publication date Collection: May 2018
                Volume: 10
                Issue: 5
                Electronic Location Identifier: 655
                Affiliations
                [1 ]Tea Research Institute, Zhejiang University, Hangzhou 310058, China; curtpolito@ 123456outlook.com (C.A.P.); 21716160@ 123456zju.edu.cn (Z.-Y.C.); 11516051@ 123456zju.edu.cn (Y.-L.S.); 21616096@ 123456zju.edu.cn (X.-M.L.); 21616106@ 123456zju.edu.cn (R.Y.); 11616052@ 123456zju.edu.cn (M.S.); qsli@ 123456zju.edu.cn (Q.-S.L.); jianhuiye@ 123456zju.edu.cn (J.-H.Y.); jllu@ 123456zju.edu.cn (J.-L.L.); xqzheng@ 123456zju.edu.cn (X.-Q.Z.)
                [2 ]Liupao Tea Academy, Wuzhou 543003, Guangxi, China; zjumasc@ 123456aliyun.com
                [3 ]National Tea and Tea product Quality Supervision and Inspection Center (Guizhou), Zunyi 563100, China; gzzyzj_2009@ 123456vip.sina.com
                [4 ]Ningbo Extension Station of Forestry & Specialty Technology, Ningbo 315012, China; wkrtea321hjytea@ 123456163.com
                Author notes
                [* ]Correspondence: yrliang@ 123456zju.edu.cn ; Tel.: +86-571-8898-2704
                Author information
                https://orcid.org/0000-0001-7889-1251
                Article
                Publisher ID: nutrients-10-00655
                DOI: 10.3390/nu10050655
                PMC ID: 5986534
                PubMed ID: 29789466
                SO-VID: fec4e027-8706-4bfc-bb9a-ccda105d4a72
                Copyright © © 2018 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 04 April 2018
                Date accepted : 21 May 2018
                Categories
                Subject: Review

                ScienceOpen disciplines: Nutrition & Dietetics
                Keywords: camellia sinensis,epigallocatechin gallate (egcg),theanine,caffeine,alzheimer’s disease,parkinson’s disease
                Data availability:
                ScienceOpen disciplines: Nutrition & Dietetics
                Keywords: camellia sinensis, epigallocatechin gallate (egcg), theanine, caffeine, alzheimer’s disease, parkinson’s disease

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