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*Compound via MeSH
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Medline Plus Health Information
*Degenerative Nerve Diseases
© 2008 American Society for Nutrition J. Nutr. 138:1578S-1583S, August 2008


Supplement: Proceedings of the Fourth International Scientific Symposium on Tea and Human Health

Targeting Multiple Neurodegenerative Diseases Etiologies with Multimodal-Acting Green Tea Catechins1,2

Silvia A. Mandel*, Tamar Amit, Limor Kalfon, Lydia Reznichenko and Moussa B. H. Youdim

Eve Topf Center for Neurodegenerative Diseases Research and Department of Pharmacology, Faculty of Medicine, Technion, Haifa, Israel

* To whom correspondence should be addressed. E-mail: mandel{at}tx.technion.ac.il.

Green tea is currently considered a source of dietary constituents endowed with biological and pharmacological activities relevant to human health. Human epidemiological and new animal data suggest that the pharmacological benefits of tea drinking may help to protect the brain as we age. Indeed, tea consumption is inversely correlated with the incidence of dementia and Alzheimer's and Parkinson's diseases. In particular, its main catechin polyphenol constituent (–)-epigallocatechin-3-gallate has been shown to exert neuroprotective/neurorescue activities in a wide array of cellular and animal models of neurological disorders. The intense efforts dedicated in recent years to shed light on the molecular mechanisms participating in the brain protective action of green tea indicate that in addition to the known antioxidant activity of catechins, the modulation of signal transduction pathways, cell survival/death genes, and mitochondrial function all contribute significantly to the induction of neuron viability. Because of the multietiological character of neurodegenerative disease pathology, these natural compounds are receiving significant attention as therapeutic cytoprotective agents that simultaneously manipulate multiple desired targets in the central nervous system. This article elaborates on the multimodal activities of green tea polyphenols with emphasis on their recently described neurorescue/neuroregenerative and mitochondrial stabilization actions.





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