Food Therapy: Green Tea Bioactive Polyphenols in Inhibited β-amyloid Accumulation in Neuro Degeneration

Kyle J. Norton 

Green tea may have a potential and therapeutic effect in protected neurons of the brain against deposit of β-amyloid in initiated neuro degenerative diseases, some researchers postulated.

β-amyloid are plaques found in the brains of Alzheimer patients derived from the amyloid precursor protein (APP) with function in binding to other proteins on the surface of cells.

Green tea, a precious drink processes numbers of health benefit known to almost everyone in Asia and Western world. However, as yin in nature herbal medicine or food, long term injection of large amounts may obstruct the balance of yin-yang, induced "yin excessive syndrome" or "yang vacuity syndrome" including weaken immunity and painful case of GERD,... according to traditional Chinese medicine's Yin-Yang theory.

The differentiation of green tea activities in risk of plagues deposit in certain parts of the brain to induce development and neuropathogenesis of dementia was found to associate to numbers of implication through several mechanisms.

In the study to clarify the effect of green tea Epigallocatechin-3-gallate (EGCG) in inhibited activities of nitrosative as well as oxidative stress in induction of Abeta-cause of damages in neurons and glial cells surround neurons, researchers at the Daegu Haany University found that application of the phytophenols exerts a significant interference in ameliorated the elevation of Abeta-induced by oxidative and/or nitrosative to facilitate cell death through its antioxidant and anti-inflammatory properties.

Further analysis found that green tea bioactive compound reduced activities of Abeta injection in induction of nitrosative stress on BV2 cells caused by increased expression of inducible nitric oxide synthase (iNOS) in production of nitric oxide (NO) and peroxynitrite, in elevated cytotoxicity to precipitate apoptosis, though inhibited reactive nitrogen species act together with reactive oxygen species to establish chain reaction in damage to BV2 cells.

In cellular metabolism, pretreatment of green tea EGCG also demonstrated a strong antioxidant properties in induction of neuroprotective effect by fortified cellular GSH over expression through elevated mRNA expression of galuatehe eva-glutamylcysteine ligase (GCL) with functions involved production of cellular antioxidant glutathione (GSH).

Additionally, the examine the inhibitory effect of l-theanine, a component of green tea (Camellia sinensis), on Abeta(1-42) with oral treatment of l-theanine (2 and 4 mg/kg) for 5 weeks in the drinking water of mice, followed by injection of Abeta(1-42) (2 microg/mouse, icv), suggested that green tea bioactive l-theanine component exerts a significantly attenuated Abeta(1-42) levels induced memory impairment by precipitated neuronal cell death in the cortex and hippocampus of the brain.

Moreover, l-theanine  also inhibited Abeta(1-42)-induced extracellular signal-regulated kinase (ERK), p38 mitogen-activated protein kinase and activity of nuclear factor kappaB (NF-kappaB) in initiated cellular apoptosis caused by reactive nitrogen species hyper activities.

 Further more, the bioactive  l-theanine also significantly reduced oxidative protein and lipid damage and elevated glutathione levels in the brain, thus reducing macromolecular oxidative damage in improved memory.

Additional study of green tea effect in attenuated accumulation of β-amyloid (Aβ) peptide plaques is a major pathogenic event in Alzheimer's disease (AD) opinionated that in the wild type amyloid precursor protein (APP) transfected (N2a/APP695) cell line, Epigallocatechin gallate (EGCG), a highly active catechin found in green tea, significantly reinforce the activity of nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ), a regulator of adipocyte differentiation by promoting its mRNA and protein expressions in N2a/APP695 cells, thus attenuated Aβ generation in N2a/APP695 cells in induction of Alzheimer's disease (AD).

Intriguingly, the efficacy of Epigallocatechin gallate (EGCG) in inhibited β-amyloid (Aβ) peptide plaques accumulation was found to be attributed by its antioxidant activity in decreased the expression of pro-apoptotic proteins (Bax, caspase-3) activated by Aβ insults,  the activity of the anti-inflammatory agent NF-κB triggered by β-amyloid (Aβ) peptide and inhibited the oxidative stress by decreasing the levels of ROS and MDA and increased the expression of antioxidant  enzyme MnSOD.

These results suggest that EGCG may have preventive and/or therapeutic potential to prevent accumulated β-amyloid in initiated neuro degenerative patients by increasing cellular antioxidant defense capacity in inhibited Abeta-mediated oxidative and/or nitrosative stress to induce cell death. Intake of green tea extract should be taken with great care, as overdoses have been reported to cause  liver toxicity.

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Author Biography
Kyle J. Norton (Scholar, Master of Nutrients, All right reserved)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published on line, including world wide health, ezine articles, article base, healthblogs, selfgrowth, best before it's news, the karate GB daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been used as references in medical research, such as international journal Pharma and Bio science, ISSN 0975-6299.

Sources
(*) Neuroprotective effect of epigallocatechin-3-gallate against beta-amyloid-induced oxidative and nitrosative cell death via augmentation of antioxidant defense capacity by Kim CY1, Lee C, Park GH, Jang JH.(PubMed)
(*) l-Theanine, an amino acid in green tea, attenuates beta-amyloid-induced cognitive dysfunction and neurotoxicity: reduction in oxidative damage and inactivation of ERK/p38 kinase and NF-kappaB pathways by Kim TI1, Lee YK, Park SG, Choi IS, Ban JO, Park HK, Nam SY, Yun YW, Han SB, Oh KW, Hong JT.(PubMed)
(*) Epigallocatechin Gallate Attenuates β-Amyloid Generation and Oxidative Stress Involvement of PPARγ in N2a/APP695 Cells by Zhang ZX1, Li YB2, Zhao RP3.(PubMed)
(1) Green tea epigallocatechin-3-gallate (EGCG) reduces beta-amyloid mediated cognitive impairment and modulates tau pathology in Alzheimer transgenic mice by Rezai-Zadeh K1, Arendash GW, Hou H, Fernandez F, Jensen M, Runfeldt M, Shytle RD, Tan J.(PubMed)