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Hello all --
Well, it might just be a coincidence but we tried the Turmeric in some Green
Tea today and the PD pain was entirely gone in about 30 minutes.  He did not
take any pain medication (Ibuprofen) or additional PD meds.  We went to the
grocery and bought Tumeric in the spice isle since we couldn't get to the
health food store today.  Tomorrow we will go there for some Curcumin in
capsule form.  We used about 1/3 of a tsp. in the tea with a little honey.
It doesn't taste bad at all.  As we said, perhaps this is just a coincidence
but we will keep you posted.

Carole and Ted (57/45/40)


----- Original Message -----
From: "Brightline" <[log in to unmask]>
To: <[log in to unmask]>
Sent: Sunday, January 30, 2005 2:02 PM
Subject: In Praise of Turmeric


> 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
> ************
> 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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