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Green tea extract may have neuroprotective effects in Parkinson's disease

  [ 29 votes ]   [ Discuss This Article ]
www.ProHealth.com • December 2, 2002


Source: The Lancet, Volume 358, Number 9279, 04 August 2001

Researchers from Israel have found that a phenolic compound in green tea is a strong neuroprotectant in two different models of Parkinson's disease. The results were presented at the 14th International Congress on Parkinson's Disease in Helsinki, Finland, on July 27, 2001.

The investigators, led by Moussa Youdim (Technion-Faculty of Medicine, Haifa, Israel), used microarrays, or "gene chips", to study the effects of epigallocatechin-3-gallate (EGCG), which comprises about a third of the polyphenol content of green tea extracts. They found that treating rodents with MPTP or 6-hydroxydopamine, the two classic inducers of experimental parkinsonism, causes a suite of 51 genes to change their expression levels, in some cases increasing by 1000% or more. These include genes for NFB, and proinflammatory cytokines, such as interleukin 1ß. However, if the rodents receive oral EGCG for 2 days before treatment, these changes in gene expression are suppressed, and the rodents are protected from the harmful effects of each toxin.

EGCG is a powerful iron chelator, which may partly explain its neuroprotective effects: iron accumulation has been implicated in a range of neurodegenerative diseases (see Lancet 2001; 358: 302), and iron accumulates in neurons in the substantia nigra of patients with Parkinson's disease.

To test the applicability of EGCG in Parkinson's disease, Youdim is currently using microarrays to see whether human brain with Parkinson's disease also shares these genetic changes. However, Youdim cautions that a long line of putative neuroprotectants have been tried, and failed, in human beings (although he is optimistic enough to have applied for a patent on EGCG). But he also notes: "Cell death is not just one process; it's a domino effect involving many pathways. I don't believe we can protect neurons with one single drug; we'll need a cocktail of agents to interrupt these different pathways."

By Richard Robinson



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