Hello Everybody:
In my daily ritual of search for a way out of pain caused by my PD, I found out to my pleasant surprise, that Curcumin or the component of common Turmeric (Curcuma longa) is a potent anti-inflammatoyr activity, more potent than ibuprophen and naxopren (?), the popular Non-steroidal anti-inflammatory drugs or NSAIDs. Curcumin also inhibits Cox-2 enzyme which is involved in the progression of PD and also in cancer growth. This is probably one of the most safe and natural NSAID one can hope for. I am thinking of discontinueing Celebrex and try Turmeric instead for the next few weeks.
To day I tried Sage tea with a pinch of tumeric and cinnamon added to it + some sugar to taste. My muscle pain disappeared within half an hour. Sage is also good for the nerves. Cinnamon has anti-infection property and also good for people with high blood presssure and diabetes.
In addition, curcumin also clears amyloid aggregation in Alzheimer Disease. Please see the abstract given below. This also helps in cognizance, a problem often met in older PD patients.
I just thought I should share this info with you. If anybody wants to try turmeric, I would like to hear their experience.
Have a nice day!
Raj
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Curcumin inhibits formation of ABeta oligomers and fibrils, bindsplaques and reduces amyloid in vivo
by Yang et al., J Biol Chem papers in press. Published Dec 7 2004.
Abstract:
Alzheimer's disease (AD) involves amyloid (ABeta) accumulation, oxidative damage and inflammation; and risk is reduced with increased anti-oxidant and anti-inflammatory consumption. The phenolic yellow curry pigment curcumin has potent anti-inflammatory and antioxidant activities and can suppress oxidative damage, inflammation, cognitive deficits, and amyloid
accumulation. Since the molecular structure of curcumin suggested potential Abeta-binding, we investigated whether its efficacy in AD models could be explained by effects on ABeta aggregation. Under aggregating conditions in vitro, curcumin inhibited aggregation (IC50 = 0.8 microM) as well as disaggregated fibrillar Abeta40 (IC50 = 1 microM), indicating favorable stoichiometry for inhibition. Curcumin was a better abeta40 aggregation inhibitor than ibuprofen and naproxen, and prevented Abeta42 oligomer formation and toxicity between 0.1-1.0 microM. under electron microscopy, curcumin decreased dose-dependently Abeta fibril formation beginning with 0.125 microM. Curcumin's effects did not depend on Abeta sequence but on fibril-related conformation. AD and Tg2576 mice brain sections incubated with curcumin revealed preferential labeling of amyloid plaques. in vivo studies showed that curcumin injected peripherally into aged Tg mice,
> crossed the blood brain barrier and bound plaques. When fed to aged Tg2576 mice with advanced amyloid accumulation, curcumin labeled plaques and reduced amyloid levels and plaque burden. hence, curcumin directly binds small beta-amyloid species to block aggregation and fibril formation in vitro and in vivo. These data suggest that low dose curcumin effectively
> disaggregates Abeta as well as prevents fibril and oligomer formation, supporting the rationale for curcumin use in clinical trials preventing or treating AD.
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