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Review
. 2018 May 29;23(6):1297.
doi: 10.3390/molecules23061297.

Beneficial Effects of Green Tea Catechins on Neurodegenerative Diseases

Affiliations
Review

Beneficial Effects of Green Tea Catechins on Neurodegenerative Diseases

Monira Pervin et al. Molecules. .

Abstract

Tea is one of the most consumed beverages in the world. Green tea, black tea, and oolong tea are made from the same plant Camellia sinensis (L.) O. Kuntze. Among them, green tea has been the most extensively studied for beneficial effects on diseases including cancer, obesity, diabetes, and inflammatory and neurodegenerative diseases. Several human observational and intervention studies have found beneficial effects of tea consumption on neurodegenerative impairment, such as cognitive dysfunction and memory loss. These studies supported the basis of tea's preventive effects of Parkinson's disease, but few studies have revealed such effects on Alzheimer's disease. In contrast, several human studies have not reported these favorable effects with regard to tea. This discrepancy may be due to incomplete adjustment of confounding factors, including the method of quantifying consumption, beverage temperature, cigarette smoking, alcohol consumption, and differences in genetic and environmental factors, such as race, sex, age, and lifestyle. Thus, more rigorous human studies are required to understand the neuroprotective effect of tea. A number of laboratory experiments demonstrated the benefits of green tea and green tea catechins (GTCs), such as epigallocatechin gallate (EGCG), and proposed action mechanisms. The targets of GTCs include the abnormal accumulation of fibrous proteins, such as Aβ and α-synuclein, inflammation, elevated expression of pro-apoptotic proteins, and oxidative stress, which are associated with neuronal cell dysfunction and death in the cerebral cortex. Computational molecular docking analysis revealed how EGCG can prevent the accumulation of fibrous proteins. These findings suggest that GTCs have the potential to be used in the prevention and treatment of neurodegenerative diseases and could be useful for the development of new drugs.

Keywords: Alzheimer’s disease; EGCG; Parkinson’s disease; brain; catechin; cognitive function; epidemiology; green tea; inflammation; neuroprotection.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Chemical structure of epigallocatechin gallate (EGCG) and related compounds.
Figure 2
Figure 2
Effect of EGCG, EGC, and gallic acid (GA) on neurite outgrowth of human neuroblastoma SH-SY5Y cells [62]. EGCG, EGC, and GA dissolved in 0.01% dimethylsulfoxide were added to the culture medium to make a final concentration of 0.05 µM and cultured for 72 h at 37 °C. Photos of (a) control cells and (b) cells treated with EGC, (c) GA, (d) EGC and GA, and (e) EGCG. (f) Neurite length and (g) neurite number of cells treated with catechins. Scale bar is 50 µm. Each value represents the mean ± SEM. Asterisks and # represent significant differences with the control (*) and with EGC and GA (#) (p < 0.05, Bonferroni’s t-test). Reproduced under Creative Commons Attribution-Noncommercial-No Derivatives License (CC BY NC ND). doi:10.1016/j.bbrep.2016.12.012.
Figure 3
Figure 3
Computational molecular docking analysis (CMDA) of the EGCG and Aβ complex [70]. The possible pose conformation of the EGCG-Aβ complex with the highest frequency is shown with the involvement of Arg5, Tyr10, and Lys16. Binding energy and the amino acid residues involved in the top five pose conformations with a high frequency are also shown. Reproduced in part with permission of the publisher, Proceedings of the National Academy of Sciences of the United States of America. doi:10.1073/pnas.12203261.

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