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09-15-2008, 07:01 AM | #1 | |||
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In Remembrance
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Just a month old. Another miracle botanical-
1: J Nutr. 2008 Aug;138(8):1578S-1583S. Targeting multiple neurodegenerative diseases etiologies with multimodal-acting green tea catechins. Mandel SA, Amit T, Kalfon L, Reznichenko L, Youdim MB. Eve Topf Center for Neurodegenerative Diseases Research and Department of Pharmacology, Faculty of Medicine, Technion, Haifa, Israel. mandel@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. PMID: 18641210 [PubMed - indexed for MEDLINE]
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Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000. Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well. |
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09-15-2008, 10:28 PM | #2 | |||
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In Remembrance
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use essential oils and drink lavender and rose tea...
spoke to a lady in the midwest who moved here from Iran, and she told me what she drank and ate for health~~~ we have been told to pop pills and without a nutrtional change, we will soon be ill again... food as medicine is a great and true concept. there is a need to integrate all medicine for healing.
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with much love, lou_lou . . by . , on Flickr pd documentary - part 2 and 3 . . Resolve to be tender with the young, compassionate with the aged, sympathetic with the striving, and tolerant with the weak and the wrong. Sometime in your life you will have been all of these. |
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09-19-2008, 04:09 PM | #3 | |||
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Youdim is one of the main developers of Azilect. He's been cheerleading green tea for PD for several years.
Also, I posted a while ago about an amazing study of egcg and prostate cancer. Participants were at very high risk of cancer within one year ( about 30%). For those on placebo, 30% did get cancer. The patients given egcg had the risk reduced by 80%! This seems to be a different study: "Taking green tea capsules virtually wiped out the development of prostate cancer in men at high risk, says Italian researcher Dr. Saverio Bettuzzi, University of Parma. He gave men 600 mg a day of concentrated green tea catechins, containing 300 mg EGCG, or a placebo for a year. All the men had premalignant lesions, putting them at risk of progression to full blown advanced and potentially fatal prostate cancer. After a year, only one man (3%) in the group on green tea capsules developed prostate cancer compared with 9 men (28%) on placebo. Thus, the green tea was nearly 90% effective in preventing prostate cancer, said researchers. They attribute the anti-cancer activity to the daily 300 mg of antioxidant EGCG. (the amount in 3 cups of brewed green tea or 1 capsule of Stop Aging Now! High-Antioxidant Green Tea Extract.) As to whether green tea's EGCG can prevent prostate cancer, "the answer is clearly yes," says Dr. Bettuzzi. (Betuzzi S. Cancer Res 2006 Jan15;66(2): 1234-40) " http://www.jeancarper.com/news/special_reports/1721 Oncogene. 2008 Mar 27;27(14):2055-63. Epub 2007 Nov 12. Green tea polyphenol EGCG sensitizes human prostate carcinoma LNCaP cells to TRAIL-mediated apoptosis and synergistically inhibits biomarkers associated with angiogenesis and metastasis. http://www.ncbi.nlm.nih.gov/pubmed/17998943 "However, only green tea is rich in the flavonol group of polyphenols known as catechins. The fermentation process used in making black tea destroys the biologically active polyphenols of the fresh leaf. The catechins as a group have significant free radical scavenging ability and are potent antioxidants. Four catechins are found in green tea leaves: epicatechin (EC) epigallocatechin (EGC) epicatechin gallate (ECG) epigallocatechin gallate (EGCG) Of these four factions EGCG is the most important to the PC patient. Pharmacological activity extends beyond its actions as an antioxidant and free radical scavenger. Epigallocatechin-3 gallate (EGCG) acts against urokinase, an enzyme often found in large amounts in human cancers (Jankun et al., Nature, 1997). Urokinase breaks down the basement membrane of cell junctions, which may be a key step in the process of tumor cell metastasis, as well as tumor growth (Ennis et al., Proc. Annu. Meet. Am. Assoc. Cancer Res., 1997). EGCG attaches to urokinase and prevents these actions." http://74.125.45.104/search?q=cache:...lnk&cd=4&gl=us "Among other targets for EGCG, urokinase is thought to enhance tumor growth in vivo by increasing the invasive and metastatic potential of cancer cells..." EGCG inhibits telomerase activity. So does circumin. So does Gleevec, which treats CML leukemia in early stages successfully. Gleevec promotes head hair growth. I wonder what enough green tea or circumin would do! Melatonin, too: http://www.ncbi.nlm.nih.gov/pubmed/1...?dopt=Abstract I think pathways in cancer relate to pathways in PD. Last edited by ZucchiniFlower; 09-19-2008 at 04:49 PM. |
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09-19-2008, 05:12 PM | #4 | |||
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Mtor pathway regulates telomerase activity. And it's involved in neurodegeneration also:
"These findings indicate that activation of the signaling network of MAPK and mTOR is associated with Cd-induced neuronal apoptosis. Our results strongly suggest that inhibitors of MAPK and mTOR may have a potential for prevention of Cd-induced neurodegeneration." http://pt.wkhealth.com/pt/re/jneu/ab...195628!8091!-1 http://mct.aacrjournals.org/cgi/content/full/2/8/789 "Rapamycin exerts its biological activity by inhibiting the kinase mammalian target of rapamycin (mTOR), which regulates important cellular processes such as control of cell cycle and cell size, translation initiation, and transcription." ....rapamycin inhibits telomerase activity ..."This suggests that the decreased hTERT transcription and loss of telomerase activity observed in our study are not merely a nonspecific consequence of cell cycle arrest but rather a specific downstream effect caused by the ability of rapamycin to inhibit the mTOR signaling pathway." |
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09-19-2008, 05:15 PM | #5 | |||
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Green tea might be related to mTOR signaling in both PD and cancer...
Role of mTOR in physiology and pathology of the nervous system Mammalian target of rapamycin (mTOR) is a serine–threonine protein kinase that regulates several intracellular processes in response to extracellular signals, nutrient availability, energy status of the cell and stress. mTOR regulates survival, differentiation and development of neurons. Axon growth and navigation, dendritic arborization, as well as synaptogenesis, depend on proper mTOR activity. In adult brain mTOR is crucial for synaptic plasticity, learning and memory formation, and brain control of food uptake. Recent studies reveal that mTOR activity is modified in various pathologic states of the nervous system, including brain tumors, tuberous sclerosis, cortical displasia and neurodegenerative disorders such as Alzheimer's, Parkinson's and Huntington's diseases. This review presents current knowledge about the role of mTOR in the physiology and pathology of the nervous system, with special focus on molecular targets acting downstream of mTOR that potentially contribute to neuronal development, plasticity and neuropathology. |
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09-19-2008, 05:21 PM | #6 | |||
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LOOKING AHEAD
While the benefits of mTOR inhibition in the treatment of cancer are obvious, regulation of mTOR activity may also be beneficial for the treatment of a number of other diseases. The mTOR Pathway as a Potential Target for the Development of Therapies Against Neurological Disease by Daniel Zemke, Seema Azhar and Arshad Majid Summary The mammalian target of rapamycin (mTOR) is a protein tyrosine kinase that regulates cell proliferation and survival via its effects on transcription, translation and autophagy. The activity of mTOR is controlled by a number of nutrient and energy sensing pathways, inhibiting cell proliferation under conditions of deprivation. In addition, mTOR has been associated with the inhibition of apoptosis and the clearance of toxic protein aggregates. Many neurodegenerative diseases are characterized by neuronal death via apoptosis, and it is possible that modulation of mTOR activity may offer some protection against their effects. In particular, diseases involving oxygen and nutrient deprivation, such as stroke, or diseases characterized by aggregate formation, such as Alzheimer's and Huntington's disease, could gain substantial benefit by either inhibiting or enhancing mTOR activity. In addition, inhibition of mTOR in cancerous tissue decreases cell proliferation and increases apoptosis, and is an effective therapy for brain tumors. In this article, the effects of mTOR and their potential usefulness for the treatment of neurological disease are examined http://journals.prous.com/journals/s...=3873&p_IsPs=Y |
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09-19-2008, 06:20 PM | #7 | |||
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How did I miss this one!?
RTP801 Is Elevated in Parkinson Brain Substantia Nigral Neurons and Mediates Death in Cellular Models of Parkinson's Disease by a Mechanism Involving Mammalian Target of Rapamycin Inactivation [mTOR] ......The mechanism by which 6-OHDA and RTP801 induce neuron death appears to involve repression of mammalian target of rapamycin (mTOR) kinase activity, and such death is inhibited by shRNAs targeting TSC2 (tuberous sclerosis complex), a protein with which RTP801 interacts to block mTOR activation. Our findings thus suggest that the elevation of RTP801 we detect in PD substantia nigral neurons may mediate their degeneration and death and that RTP801 and its signaling cascade may be novel potential therapeutic targets for the disease. http://www.jneurosci.org/cgi/content...act/26/39/9996 |
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09-19-2008, 09:26 PM | #8 | |||
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http://www.realage.com/ct/eat-smart/food-and-nutrition/tip/6890
Quote:
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_________________________________________________ http://calipso-pd.org ...bringing a new wave of Parkinson’s support to central Illinois |
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09-21-2008, 08:20 PM | #9 | |||
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In Remembrance
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with much love, lou_lou . . by . , on Flickr pd documentary - part 2 and 3 . . Resolve to be tender with the young, compassionate with the aged, sympathetic with the striving, and tolerant with the weak and the wrong. Sometime in your life you will have been all of these. Last edited by lou_lou; 09-22-2008 at 01:07 AM. |
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