Cited by 74Alzheimer's disease research and treatmentsTea Polyphenols and EffectsMedicinal Plants and Neuroprotection

The Pharmacological Activity of Epigallocatechin-3-Gallate (EGCG) on Alzheimer's Disease Animal Model: A Systematic Review

Zhang, Shuang, Zhu, Qi, Chen, Jia-Yue, OuYang, Defang, Lu, Jia-Hong·2020·Phytomedicine

Abstract

Background Alzheimer's disease (AD) is currently incurable and there is an urgent need to develop new AD drugs. Many studies have revealed the potential neuroprotective effect of Epigallocatechin-3-O-gallate (EGCG), the main antioxidant in green tea, on animal models of AD. However, a systematic review of these reports is lacking.Purpose To assess the effectiveness of EGCG for AD treatment using systematic review and meta-analysis of pre-clinical trials.Methods We conducted a systematic search of all available randomized controlled trials (RCTs) performed up to November 2019 in the following electronic databases: ScienceDirect, Web of Science, and PubMed. 17 preclinical studies assessing the effect of EGCG on animal AD models have been identified. Meta-analysis and subgroup analysis was performed to evaluate cognition improvement of various types of AD models. The study quality was assessed using the CAMARADES checklist and the criteria of published studies.Results Our analysis shows that the methodological quality ranges from 3 to 5, with a median score of 4. According to meta-analysis of random-effects method, EGCG showed a positive effect in AD with shorter escape latency (SMD= -9.24, 95%CI= -12.05 to -6.42) and decreased Aβ 42 level (SD= -25.74,95%CI= -42.36 to -9.11). Regulation of α-, β-, γ-secretase activity, inhibition of tau phosphorylation, anti-oxidation, anti-inflammation, anti-apoptosis, and inhibition of AchE activity are reported as the main neuroprotective mechanisms. Though more than 100 clinical trials have been registered on the ClinicalTrials.gov, only one clinical trial has been conducted to test the therapeutic effects of EGCG on the AD progression and cognitive performance.Conclusion Here, we conducted this review to systematically describe the therapeutic potential of EGCG in animal models of AD and hope to provide a more comprehensive assessment of the effects in order to design future clinical trials. Besides, the safety, blood-brain barrier (BBB) penetration and bioavailability issues in conducting clinical trials were also discussed.

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Crossref · 10.1016/j.phymed.2020.153316

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  • EGCG can rescue cognitive impairment and Aβ pathology in animal models of AD through anti-inflammatory, antioxidant, and antiaggregating activities.

    “A recent meta-analysis of 17 studies performed on animal models of AD has demonstrated that EGCG can rescue cognitive impairment and Aβ pathology through the combination of its anti-inflammatory, antioxidant, and antiaggregating activities (Zhang et al., 2020)”

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Authors
Zhang, S., Zhu, Q., Chen, J.-Y., OuYang, D., & Lu, J.-H.
Affiliations
University of Macau (MO)
Venue
Phytomedicine
Publisher
Elsevier BV
Published
2020-12
Volume
79
Pages
153316
ISSN
0944-7113 (ISSN-L)
OpenAlex
W3082727968
Cited by
74
References
67
Citations by year
2026: 9 · 2025: 10 · 2024: 12 · 2023: 14 · 2022: 12 · 2021: 16
FWCI
1.34
Type
journal article
Language
en
Open access
closed
Locations
  • Phytomedicine (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Tea Polyphenols and Effects
  • Health Sciences › Medicine › Complementary and alternative medicine › Medicinal Plants and Neuroprotection
Keywords
epigallocatechin gallate, Alzheimer's disease, green tea, neuroprotection, animal models of Alzheimer's disease, cognitive impairment, tau phosphorylation, antioxidant activity, anti-inflammatory activity, acetylcholinesterase inhibition, blood-brain barrier penetration, bioavailability, clinical translation
MeSH terms
Alzheimer Disease, Animals, Antioxidants, Blood-Brain Barrier, Catechin, Cognition, Disease Models, Animal, Humans, Phosphorylation, Neuroprotective Agents, Amyloid Precursor Protein Secretases

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