FAQ/Help |
Calendar |
Search |
Today's Posts |
09-15-2008, 07:01 AM | #1 | |||
|
||||
In Remembrance
|
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]
__________________
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. |
|||
Reply With Quote |
|
|
Similar Threads | ||||
Thread | Forum | |||
Trophos SA Receives Grant From The MJF Foundation To Eval Compounds In PD Model | Parkinson's Disease | |||
Stress & Neurodegeneration | Parkinson's Disease | |||
Antioxidant compounds have potent anti-fibrillogenic and fibril- | Parkinson's Disease | |||
Marijuana-like compounds may aid ALS | ALS |