Raj - Here in Houston, we have a pharmacist who is more inclined to
natural meds to help people.  He writes for the Houston Chronicle.  One
day he wrote a nice informative article about the components of tumeric
or cumin and how it helps arthritis.  I haven't tried it yet, but I'm
getting close to needing to try it.  Best to you.  Jo Ann

On Sun, 30 Jan 2005 18:02:15 -0400 Brightline
<[log in to unmask]> writes:
> 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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