J Neurochem. 2004 Mar;88(6):1555-69.  Links

Cell signaling pathways in the neuroprotective actions of the green tea
polyphenol (-)-epigallocatechin-3-gallate: implications for neurodegenerative
diseases.

Mandel S, Weinreb O, Amit T, Youdim MB.

Eve Topf and USA National Parkinson Foundation Centers of Excellence for
Neurodegenerative Diseases Research and Department of Pharmacology,
Technion-Faculty of Medicine, Haifa, Israel.

Accumulating evidence supports the hypothesis that brain iron misregulation and
oxidative stress (OS), resulting in reactive oxygen species (ROS) generation
from H2O2 and inflammatory processes, trigger a cascade of events leading to
apoptotic/necrotic cell death in neurodegenerative disorders, such as
Parkinson's (PD), Alzheimer's (AD) and Huntington's diseases, and amyotrophic
lateral sclerosis (ALS). Thus, novel therapeutic approaches aimed at
neutralization of OS-induced neurotoxicity, support the application of ROS
scavengers, transition metals (e.g. iron and copper) chelators and non-vitamin
natural antioxidant polyphenols, in monotherapy, or as part of antioxidant
cocktail formulation for these diseases. Both experimental and epidemiological
evidence demonstrate that flavonoid polyphenols, particularly from green tea
and blueberries, improve age-related cognitive decline and are neuroprotective
in models of PD, AD and cerebral ischemia/reperfusion injuries. However, recent
studies indicate that the radical scavenger property of green tea polyphenols
is unlikely to be the sole explanation for their neuroprotective capacity and
in fact, a wide spectrum of cellular signaling events may well account for
their biological actions. In this article, the currently established mechanisms
involved in the beneficial health action and emerging studies concerning the
putative novel molecular neuroprotective activity of green tea and its major
polyphenol (-)-epigallocatechin-3-gallate (EGCG), will be reviewed and
discussed.

PMID: 15009657 [PubMed - in process]

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