Curcumin, the major component of the spice turmeric and the yellow pigment in curry powder, has several properties that make it of interest as a possible anti-TSE drug. First, its structure resembles Congo red, the most potent of the small-molecule PrP-res inhibitors that have been assayed in ScNB cells in that both are potentially planar compounds that have two aromatic rings or ring systems with conjugated linkers. Structure-activity studies have provided evidence that the potential for coplanarity of the rings and linker is important for the inhibitory potency of Congo red . Second, unlike Congo red, curcumin is uncharged and is thought to have at least limited bioavailability to the brain after consumption. Indeed, recent studies with a rat model of Alzheimer's disease reported that dietary curcumin reduces ß-peptide deposition in the brain as well as associated neuropathology and cognitive deficits. Third, curcumin has antioxidant activity, a factor that may be important given that oxidative damage is a feature in TSE neuropathogenesis. Fourth, humans consume curcumin in large amounts with no apparent toxicity. Toxicology studies have indicated that rodents can tolerate for a long period up to 5% of their diet being turmeric oleoresin (80% curcumin) without their life spans being shortened (http://ntp-server.niehs.nih.gov/htdocs/LT-studies/tr427.html). These considerations prompted us to test whether curcumin could inhibit the formation and accumulation of PrP-res. More
See, here at pure bs, we are curious about a great many things. Honest!
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