Cited by 460Alzheimer's disease research and treatmentsTea Polyphenols and EffectsMedicinal Plants and Neuroprotection

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Green tea epigallocatechin-3-gallate (EGCG) reduces β-amyloid mediated cognitive impairment and modulates tau pathology in Alzheimer transgenic mice

Abstract

We previously reported that intraperitoneal (i.p.) injection (20 mg/kg) of (-)-epigallocatechin-3-gallate (EGCG), the main polyphenolic constituent of green tea, decreased beta-amyloid (Abeta) levels and plaques via promotion of the non-amyloidogenic alpha-secretase proteolytic pathway in "Swedish" mutant amyloid precursor protein overexpressing (APPsw, Tg) mice. Here, we find that EGCG administered orally in drinking water (50 mg/kg) similarly reduces Abeta deposition in these mice. Following a six month treatment of an 8 month old cohort, immunohistochemical analysis of coronal sections reveals that plaque burdens were reduced in the cingulate cortex, hippocampus, and entorhinal cortex by 54%, 43%, and 51%, respectively. Congo red plaque burdens were decreased in the cingulate cortex, hippocampus, and entorhinal cortex by 53%, 53%, and 58%, respectively as well. ELISA of brain homogenates of the treatment Tg mice revealed consistent reductions in both Abeta1-40 and 1-42 soluble and insoluble forms. In the present study we also investigated the effect EGCG administration had on tau pathology and cognition in Tg mice. Both i.p. and orally-treated Tg animals were found to have modulated tau profiles, with markedly suppressed sarkosyl-soluble phosphorylated tau isoforms. Radial arm water maze (RAWM) testing for working memory indicated that EGCG provided cognitive benefit to Tg mice with both i.p. and oral administration, although i.p.-treated animals showed a more pronounced benefit because of the greater impairment of their Tg controls at the time of testing. Taken together, these data further the notion of EGCG dietary supplementation as a potentially safe and effective prophylaxis for Alzheimer's disease.

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Crossref · 10.1016/j.brainres.2008.02.107

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Metadata

Authors
Rezai-Zadeh, K., Arendash, G. W., Hou, H., Fernandez, F., Jensen, M., Runfeldt, M., Shytle, R. D., & Tan, J.
Affiliations
  • University of South Florida (US)
  • USF Health Byrd Alzheimer's Institute (US)
Corresponding author
Tan, Jun
Venue
Brain Research
Publisher
Elsevier BV
Published
2008-06
Volume
1214
Pages
177-187
ISSN
0006-8993 (ISSN-L)
OpenAlex
W2052380265
Cited by
459
References
50
Citations by year
2026: 14 · 2025: 28 · 2024: 17 · 2023: 26 · 2022: 27 · 2021: 30 · 2020: 37 · 2019: 20 · 2018: 28 · 2017: 31 · 2016: 20 · 2015: 27 · 2014: 27 · 2013: 33 · 2012: 32
FWCI
13.81
Type
journal article
Language
en
Open access
closed
Locations
  • Brain Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Institute on Aging (AG04418, P01AG004418, R21AG031037, P50AG025711, AG025711, AG031037)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
  • Life Sciences › Agricultural and Biological Sciences › Food Science › Tea Polyphenols and Effects
  • Health Sciences › Medicine › Complementary and alternative medicine › Medicinal Plants and Neuroprotection
Keywords
epigallocatechin gallate, green tea polyphenols, Alzheimer's disease, amyloid plaques, tau phosphorylation, oral administration, working memory, cognitive impairment, dietary supplementation, neuroprotection
MeSH terms
Alzheimer Disease, Analysis of Variance, Animals, Catechin, Cognition Disorders, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Mice, Transgenic, Mutation, Phosphorylation, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, tau Proteins, Neuroprotective Agents, Maze Learning, Mice

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