tomorrows news today, page-9

Hi Maslow, found it.
[While tau knockout mice performed as well as their wild-type littermates at six months on a variety of motor tasks, by 12 months they moved slower, took longer to turn, and fell from a rotating rod faster. The aged mice had lost 40 percent of their substantia nigra dopamine neurons, and their motor deficits could be overcome by administering levodopa. That's a very good definition of a Parkinson disease model, Dr. Bush said.
The tau knockout mice shared another feature with PD patients and MPTP-treated mice they accumulated iron in their substantia nigras as they aged. Iron has been suggested as a key instigator of oxidative damage and neuronal death in a number of neurodegenerative diseases, and in cell culture, Dr. Bush's team showed that neurons without tau were more susceptible to iron toxicity, succumbing at lower iron levels that neurons that express tau. It seems like tau is playing some role in defending the tissue against the effects of iron elevation, Dr. Bush said.
To test whether iron accumulation was in fact pathogenic, the researchers treated the knockout mice with an iron chelator and ionophore, clioquinol. Performance on the turning test was normalized in treated mice, even when the treatment was begun after the onset of symptoms. It was a really striking rescue, Dr. Bush said. It prevents them from deteriorating with age, and even when they have deteriorated, it can recover them. That was really a surprising result. It indicates the drug is addressing an underlying problem, which we believe is iron accumulation.]

http://journals.lww.com/neurotodayonline/Fulltext/2011/01060/Loss_of_Tau_Increases_Iron,_Causes_Parkinsonism.6.aspx

I believe the Parkinsons drug is close to entering the clinic. I dont know what the market for Parkinsons is worth, but I would think it has blockbuster potential. From the above, if it works I doubt it will take long to prove. Also I havnt researched yet if Parkinsons has Orphan Drug rating.