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Dietary supplementation of a high-temperature-processed green tea extract attenuates cognitive impairment in PS2 and Tg2576 mice

Kim, Juewon, Funayama, Shinichiro, Izuo, Naotaka, Shimizu, Takahiko·2019·Bioscience, Biotechnology, and Biochemistry

Abstract

Green tea intake is generally recognized as an effective supplement that promotes mental clarity and cognitive function. These health benefits of green tea have been attributed mainly to its effective component, epigallocatechin gallate (EGCG). Because various catechin derivatives potently enhance these health benefits, we manipulated the extraction process with a high-temperature intervention. High-temperature-processed green tea extract (HTP-GTE) showed an elevated proportion of gallocatechin gallate (GCG) content. To investigate the preventive effects of HTP-GTE on cognitive decline, we found its neuroprotective effects against amyloid β (Aβ)-induced neurotoxicity in neurons and clarified that GCG significantly inhibited Aβ aggregation in vitro. Moreover, we showed that HTP-GTE intake attenuated several cognitive-decline phenotypes in a model mouse of Alzheimer’s disease. These beneficial effects of HTP-GTE against cognitive decline were due to the distinctive composition of the extract and suggest the possibility that HTP-GTE supplementation could attenuate cognitive decline of Alzheimer’s disease.

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Research works printed but not linked: 38

  1. Lin, 2017, Genetic biomarkers on age-related cognitive decline, Front Psychiatry, 8, 247, 10.3389/fpsyt.2017.00247 · DOI
  2. Anderson, 2017, 50 years of cognitive aging theory, J Gerontol B Psychol Sci Soc Sci, 72, 1, 10.1093/geronb/gbw108 · DOI
  3. Spence, 2017, A brief review of three common supplements used in Alzheimer’s disease, J Am Soc Consultant Pharm, 32, 412, 10.4140/TCP.n.2017.412 · doi:10.4140/tcp.n.2017.412
  4. Schmidt, 2014, Green tea extract enhances parieto-frontal connectivity during working memory processing, Psychopharmacology (Berl), 231, 3879, 10.1007/s00213-014-3526-1 · DOI · Paper page
  5. Borgwardt, 2012, Neural effects of green tea extract on dorsolateral prefrontal cortex, Eur J Clin Nutr, 66, 1187, 10.1038/ejcn.2012.105 · DOI · Paper page
  6. Tomata, 2012, Green tea consumption and the risk of incident functional disability in elderly Japanese: the Ohsaki Cohort 2006 study, Am J Clin Nutr, 95, 732, 10.3945/ajcn.111.023200 · DOI
  7. Feng, 2016, Tea consumption reduces the incidence of neurocognitive disorders: findings from the Singapore longitudinal aging study, J Nutr Health Aging, 20, 1002, 10.1007/s12603-016-0687-0 · DOI
  8. Kuriyama, 2006, Green tea consumption and cognitive function: a cross-sectional study from the Tsurugaya project 1, Am J Clin Nutr, 83, 355, 10.1093/ajcn/83.2.355 · DOI · Paper page
  9. Rezai-Zadeh, 2005, Green tea epigallocatechin-3-gallate (EGCG) modulates amyloid precursor protein cleavage and reduces cerebral amyloidosis in Alzheimer transgenic mice, J Neurosci, 25, 8807, 10.1523/JNEUROSCI.1521-05.2005 · DOI · Paper page
  10. Du, 2018, Epigallocatechin gallate reduces amyloid beta-induced neurotoxicity via inhibiting endoplasmic reticulum stress-mediated apoptosis, Mol Nutr Food Res, 62, e1700890, 10.1002/mnfr.201700890 · DOI
  11. Jia, 2013, (-)-Epigallocatechin-3-gallate alleviates spatial memory impairment in APP/PS1 mice by restoring IRS-1 signaling defects in the hippocampus, Mol Cell Biochem, 380, 211, 10.1007/s11010-013-1675-x · DOI
  12. Liu, 2014, (-)-Epigallocatechin-3-gallate ameliorates learning and memory deficits by adjusting the balance of TrkA/p75NTR signaling in APP/PS1 transgenic mice, Mol Neurobiol, 49, 1350, 10.1007/s12035-013-8608-2 · DOI
  13. Ishino, 2010, Epimerization of tea catechins under weakly acidic and alkaline conditions, Biosci Biotechnol Biochem, 74, 875, 10.1271/bbb.90884 · doi:10.1271/bbb.90884
  14. Jeong, 2018, Transport of gallocatechin gallate and catechin gallate in high-temperature-processed green tea extract from gastrointestinal tract to brain by an in vitro bio-mimic model system coupled with sequential cell cultures, J Funct Foods, 47, 83, 10.1016/j.jff.2018.05.028 · DOI
  15. Hsiao, 1996, Correlative memory deficits, abeta elevation, and amyloid plaques in transgenic mice, Science (New York, NY), 274, 99, 10.1126/science.274.5284.99 · DOI · Paper page
  16. Toda, 2011, Presenilin-2 mutation causes early amyloid accumulation and memory impairment in a transgenic mouse model of Alzheimer’s disease, J Biomed Biotechnol, 2011, 617974, 10.1155/2011/617974 · DOI
  17. Izuo, 2017, A Toxic conformer of Abeta42 with a turn at 22-23 is a novel therapeutic target for Alzheimer’s Disease, Sci Rep, 7, 11811, 10.1038/s41598-017-11671-6 · DOI
  18. Obregon, 2006, ADAM10 activation is required for green tea (-)-epigallocatechin-3-gallate-induced alpha-secretase cleavage of amyloid precursor protein, J Biol Chem, 281, 16419, 10.1074/jbc.M600617200 · DOI · Paper page
  19. Van der Borght, 2007, Exercise improves memory acquisition and retrieval in the Y-maze task: relationship with hippocampal neurogenesis, Behav Neurosci, 121, 324, 10.1037/0735-7044.121.2.324 · DOI · Paper page
  20. Kinnavane, 2015, Advances in the behavioural testing and network imaging of rodent recognition memory, Behav Brain Res, 15, 67, 10.1016/j.bbr.2014.07.049 · DOI
  21. Lovestone, 2000, Fleshing out the amyloid cascade hypothesis: the molecular biology of Alzheimer’s disease, Dialogues Clin Neurosci, 2, 101, 10.31887/DCNS.2000.2.2/slovestone · DOI
  22. Polito, 2018, association of tea consumption with risk of Alzheimer’s disease and anti-beta-amyloid effects of tea, Nutrients, 10, 10.3390/nu10050655 · DOI
  23. Lee, 2018, Effect of catechins and high-temperature-processed green tea extract on scavenging reactive oxygen species and preventing Abeta1-42 fibrils’ formation in brain microvascular endothelium, Nutr Neurosci, 15, 1
  24. Izuo, 2013, Non-toxic conformer of amyloid beta may suppress amyloid beta-induced toxicity in rat primary neurons: implications for a novel therapeutic strategy for Alzheimer’s disease, Biochem Biophys Res Commun, 438, 1, 10.1016/j.bbrc.2013.05.106 · DOI
  25. Ehrnhoefer, 2008, EGCG redirects amyloidogenic polypeptides into unstructured, off-pathway oligomers, Nat Struct Mol Biol, 15, 558, 10.1038/nsmb.1437 · DOI · Paper page
  26. Hudson, 2009, (-)-epigallocatechin-3-gallate (EGCG) maintains kappa-casein in its pre-fibrillar state without redirecting its aggregation pathway, J Mol Biol, 392, 689, 10.1016/j.jmb.2009.07.031 · DOI
  27. Reinke, 2007, Structure-activity relationships of amyloid beta-aggregation inhibitors based on curcumin: influence of linker length and flexibility, Chem Biol Drug Des, 70, 206, 10.1111/j.1747-0285.2007.00557.x · DOI · Paper page
  28. Murakami, 2012, Stimulation of the amyloidogenic pathway by cytoplasmic superoxide radicals in an Alzheimer’s disease mouse model, Biosci Biotechnol Biochem, 76, 1098, 10.1271/bbb.110934 · DOI
  29. Murakami, 2011, SOD1 (copper/zinc superoxide dismutase) deficiency drives amyloid beta protein oligomerization and memory loss in mouse model of Alzheimer disease, J Biol Chem, 286, 44557, 10.1074/jbc.M111.279208 · DOI · Paper page
  30. Oikonomidi, 2016, Homocysteine metabolism is associated with cerebrospinal fluid levels of soluble amyloid precursor protein and amyloid beta, J Neurochem, 139, 324, 10.1111/jnc.13766 · DOI
  31. Koss, 2016, Soluble pre-fibrillar tau and beta-amyloid species emerge in early human Alzheimer’s disease and track disease progression and cognitive decline, Acta Neuropathol, 132, 875, 10.1007/s00401-016-1632-3 · DOI · Paper page
  32. Wang, 2017, Oligomeric forms of amyloid-beta protein in plasma as a potential blood-based biomarker for Alzheimer’s disease, Alzheimer’s Res Ther, 9, 98, 10.1186/s13195-017-0324-0 · DOI
  33. Lee, 1998, A detergent-insoluble membrane compartment contains A beta in vivo, Nat Med, 4, 730, 10.1038/nm0698-730 · DOI · Paper page
  34. Petrushina, 2007, Alzheimer’s disease peptide epitope vaccine reduces insoluble but not soluble/oligomeric Abeta species in amyloid precursor protein transgenic mice, J Neurosci, 27, 12721, 10.1523/JNEUROSCI.3201-07.2007 · DOI
  35. Lavretsky, 2016, Lifestyle medicine for prevention of cognitive decline: focus on green tea, Am J Geriatric Psychiatry, 24, 890, 10.1016/j.jagp.2016.08.002 · DOI
  36. Wu, 2012, Pharmacokinetics and blood-brain barrier penetration of (+)-catechin and (-)-epicatechin in rats by microdialysis sampling coupled to high-performance liquid chromatography with chemiluminescence detection, J Agric Food Chem, 60, 9377, 10.1021/jf301787f · DOI
  37. Huebbe, 2010, Effect of dietary quercetin on brain quercetin levels and the expression of antioxidant and Alzheimer’s disease relevant genes in mice, Pharmacol Res, 61, 242, 10.1016/j.phrs.2009.08.006 · DOI
  38. Farr, 2003, The antioxidants alpha-lipoic acid and N-acetylcysteine reverse memory impairment and brain oxidative stress in aged SAMP8 mice, J Neurochem, 84, 1173, 10.1046/j.1471-4159.2003.01580.x · DOI · Paper page

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Metadata

Authors
Kim, J., Funayama, S., Izuo, N., & Shimizu, T.
Affiliations
Department of Endocrinolog, Hematology, and Geriatrics, Chiba University Graduate School of Medicine, Chiba, Japan
Venue
Bioscience, Biotechnology, and Biochemistry
Published
2019-12-02
Volume
83
Issue
12
Pages
2364-2371
ISSN
  • 0916-8451
  • 1347-6947
Cited by
19
References
7
Language
en

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Kim, J., Funayama, S., Izuo, N., & Shimizu, T. (2019). Dietary supplementation of a high-temperature-processed green tea extract attenuates cognitive impairment in PS2 and Tg2576 mice. Bioscience, Biotechnology, and Biochemistry. https://doi.org/10.1080/09168451.2019.1659721

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