Green tea may have a potential effect in the regulation of Lewy bodies against the onset of Lewy body disease, some scientists suggested.
Lewy body disease is one of a common form of neurodegenerative diseases occurring in the elderly characterized by mutation of the Lewy bodies as a result of the abnormal structure of Lewy bodies, building up in areas of the brain.
Lewy bodies, mainly composed of α-synuclein (αS), are pathological hallmarks of Parkinson's disease and dementia with Lewy bodies.
People with building up of Lewy body in most cases also have Alzheimer's disease, causing reduced mental ability, including symptoms of visual hallucinations, and changes in alertness and attention.
Some patients with the condition are also experiencing symptoms of rigid muscles, slow movement, and tremors, the hallmarks of Parkinson's disease.
Researchers do not know why the elderly with the same health conditions and family history, some are susceptible to the early onset of the disease while others do not. However, they do know that certain risk factors such as old age, family history, and male gender are associated with the onset of Lewy body disease.
Some researchers also believe due to the severity of brain damage, patients with the condition also express certain mental instability including aggressive behavior, depression and worsening of parkinsonian-like symptoms.
A genetic alternation such as SNCA or SNCB gene mutations is also found in patients with the disease.
According to the My Virtual Medical Center, Lewy bodies is the third most frequent cause of dementia in older adults and accounts for 15–35% of all dementias
Green tea, a precious drink processes number of health benefits known to almost everyone in Asia and the Western world.
In the study of N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)- and 6-hydroxydopamine-induced neurodegeneration in rodents and nonhuman primates with the increased presence of iron and alpha-synuclein in the SNpc, researchers found that application of green tea catechin polyphenol (-)-epigallocatechin-3-gallate exerts a significant effect as an iron chelator in protecting the brain against neurotoxins by inhibiting the increased presence of iron and alpha-synuclein in the SNpc.
Pretreatment of green tea on N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)- and 6-hydroxydopamine-induced neurodegeneration in rodents was also found to demonstrate the high levels of antioxidant activity in preventing the accumulation of iron and alpha-synuclein in SNpc.
Dr. Mandel S, the lead author suggested that a combination of iron chelation and antioxidant therapy might be a significant approach to neuroprotection in PD and other neurodegenerative diseases, including Lewy body disease.
Furthermore, in the concerns of the primary α-synucleinopathgenic expression in patients with Parkinson's disease (PD), dementia with Lewy bodies and multiple system atrophy, researchers at the Lanzhou University, launched an investigation to examine whether green tea (-)-Epigallocatechin-3-gallate (EGCG) can inhibit the fibrillation of αS.
After taking into account co and confounders, researchers showed that
* EGCG displays a potential effect in remodeling the αS fibrils and breaking the initially ordered pattern by reducing the β-sheet content.
* EGCG can also break the Greek confirmation of αS by the disappeared H-bond in the secondary structure of turn.
Dr. Liu X, the lead author at the end of the study said, "The results from our study can not only reveal the specific interaction between EGCG and β-sheet-rich fibrils of αS, but also provide useful guidance for the discovery of other potential inhibitors".
In other words, green tea EGCG may be considered a primary target for extracting the pharmaceutical inhibitor for the treatment of Lewy body disease.
Moreover, in the differentiation of the EGCG effect in patients with Lewy body disease, researchers at the Kanazawa University Graduate School of Medical Science conducted an evaluation to examine
EGCG effect on the transient 'active' oligomers (AOs),
At the final report, researchers found that
* EGCG facilitates the fibril formation and thus eliminating the toxic AOs.
* Also, EGCG suppresses the membrane disrupting radiating amyloid fibril formation on the surface of liposomal membranes, thus protecting the cells against the initiation of AOs.
Dr. Yang JE, the lead wrote in the summary," EGCG has been suggested to exhibit its protective effect against the αS-mediated cytotoxicity by not only producing the off-pathway 'compact' oligomers but also facilitating the conversion of 'active' oligomers into amyloid fibrils".
Taken altogether, green tea and its bioactive compound EGCG may have a potential effect in treating Lewy body disease by preventing the overexpression of α-synuclein (αS) accumulation in the brain by either inhibiting the oligomers or converting the oligomers into amyloid fibrils.
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Author Biography
Kyle J. Norton (Scholar, Master of Nutrition, All right reserved)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published online, including worldwide health, ezine articles, article base, health blogs, self-growth, 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 Bioscience, ISSN 0975-6299.
Sources
(1) Iron and alpha-synuclein in the substantia nigra of MPTP-treated mice: effect of neuroprotective drugs R-apomorphine and green tea polyphenol (-)-epigallocatechin-3-gallate by Mandel S1, Maor G, Youdim MB. (PubMed)
(2) EGCG-mediated Protection of the Membrane Disruption and Cytotoxicity Caused by the 'Active Oligomer' of α-Synuclein by Yang JE1, Rhoo KY2, Lee S1, Lee JT1, Park JH1, Bhak G1, Paik SR(PubMed)
(3) Influence of EGCG on α-synuclein (αS) aggregation and identification of their possible binding mode: A computational study using molecular dynamics simulation by Liu X1, Zhou S1,2, Shi D1, Bai Q1, Liu H2, Yao X1.(PubMed)
(4) Alpha-synuclein biology in Lewy body diseases by Woojin Scott Kim, Katarina Kågedal and Glenda Halliday (Research Gate)
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