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Tiana Castiglione—McMaster Honours Life Sciences 2026

Alzheimer’s disease (AD) is characterized by the progressive deterioration of cognitive function. This fatal disease, resulting in memory loss, is the most common cause of dementia.¹ In 2017, there were approximately 76,000 new dementia cases per year, accounting for an AD prevalence of 7.1%.¹ It is anticipated that these numbers will increase in the near future.²

The accumulation of β-amyloid peptide (Aβ) in the brain is a primary characteristic of AD.¹ Interestingly, recent studies have shown that green tea is an effective therapeutic agent in both treating and preventing AD through monitoring Aβ levels.¹ Green tea contains an ester group, operating as a bioactive polyphenol called epigallocatechin-3-gallate (EGCG).¹ Contrary to fully fermented tea, green tea preserves its original polyphenolic compositions, therefore having  important antioxidant, anti-inflammatory, antidiabetic, anticarcinogenic and antineurodegenerative properties.¹ This review focuses on the latter property of neuroprotection as a result of EGCG in green tea.¹

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In a study conducted by Youn et al., EGCG treatment was administered in amyloid precursor protein (APP) transgenic mouse models for 3 months.It was demonstrated that only 40% of the initial Aβ buildup was left in the front cortex, and 48% left in the hippocampus.¹ These results are consistent with another study conducted by Rezai-Zadeh et al., where it was found that when EGCG was injected intraperitoneally, it was able to reduce Aβ deposition in transgenic APP mouse models.³ Similar effects were perceived in these mouse models when EGCG was administered orally in drinking water.³

Moreover, EGCG has also been shown to reduce the onset of Aβ-generated mitochondrial impairment and oxidative stress.¹ This was seen in both cellular and mouse models, where EGCG decreased lipid peroxidation in hippocampal neurons, thereby inhibiting Aβ-caused impairment.¹ For instance, oral administration of green tea extract over a 26-week period depressed reactive oxygen species concentrations in the hippocampus and lipid peroxides in the plasma of rats, in addition to regenerating mitochondrial function and ATP levels in mice.¹ This reduction in Aβ accumulation results in a lower risk of AD onset.

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EGCG especially holds promise for the prevention of AD given its permeability of the blood-brain barrier (BBB).¹ The BBB is a barrier that prevents certain compounds from entering the brain tissue from the blood.¹ In order for neuroprotective agents to be effective, they must have the ability to cross the BBB.¹ After consumption, a proportion of EGCG appeared to successfully enter the bloodstream in humans and rats.¹

In summary, the neuroprotective role that green tea provides through increased levels of EGCG occurs in the inhibition of Aβ accumulation via controlling amyloid precursor protein processing, as well as the attenuation of Aβ-induced oxidative stress and neuroinflammatory response.¹ However, although the properties of EGCG as a therapeutic agent and its BBB permeability are promising in preventing AD, additional research and human clinical trials are required to substantiate the potency of EGCG as a neuroprotectant.¹

References

1. Youn K, Ho C, Jun M. Multifaceted neuroprotective effects of (-)-epigallocatechin-3-gallate (EGCG) in Alzheimer’s disease: an overview of pre-clinical studies focused on β-amyloid peptide. Food Sci Hum Wellness [Internet]. 2022 [cited 2022 Nov 21];11(3):483-493. Available from: https://www.sciencedirect.com/science/article/pii/S2213453021001348 doi: 10.1016/j.fshw.2021.12.006

2. Public Health Agency of Canada. Dementia in Canada, including Alzheimer’s disease [Internet]. Government of Canada; 2017 [updated 2017 Sep 29; cited 2022 Nov 21]. Available from: https://www.canada.ca/en/public-health/services/publications/diseases-conditions/dementia-highlights-canadian-chronic-disease-surveillance.html

3. Cascella M, Bimonte S, Muzio MR, Schiavone V, Cuomo A. The efficacy of Epigallocatechin-3-gallate (green tea) in the treatment of Alzheimer’s disease: an overview of pre-clinical studies and translational perspectives in clinical practice. Infect Agents Cancer [Internet]. 2017 [cited 2022 Nov 21];12(36). Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5477123/ doi: 10.1186/s13027-017-0145-6

4. Singh NA, Mandal AKA, Khan ZA. Potential neuroprotective properties of epigallocatechin-3-gallate (EGCG). Nutr J [Internet]. 2016 [cited 2022 Nov 21];15(60). Available from: https://nutritionj.biomedcentral.com/articles/10.1186/s12937-016-0179-4 doi: https://doi.org/10.1186/s12937-016-0179-4