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Old 12-21-2008, 11:51 PM
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reverett123 reverett123 is offline
In Remembrance
 
Join Date: Aug 2006
Posts: 3,772
15 yr Member
reverett123 reverett123 is offline
In Remembrance
reverett123's Avatar
 
Join Date: Aug 2006
Posts: 3,772
15 yr Member
Default Going to bring this back to life

I was quite excited about this and was trying to understand it here in public when I received a PM from a friend telling me that I had put my big foot down right in the middle of some very sensitive negotiations over patent issues that needed to be resolved to move it toward clinical trials.

I have now been told that those negotiations have gone well and that trials should begin this year! And that it is safe to talk about it again. So, it being Christmas, a little hope for us all makes a good present.

I know more than I did, so I am going to try to clear up some of the confusion. First, we are talking about two different but similar discoveries by the same team led by P.S. Whitton. One is that urocortin acting upon CRF receptors triggered repair. Unfortunately, urocortin does not cross the BBB, plus there are a lot of unknowns about it to be followed up.

The other, and far more exciting, was the discovery that the receptors for a peptide called Glucagon-Like Peptide-1 (GLP-1) triggered similar repair when activated by either GLP-1 itself or an agonist (mimic). The diabetic drug Ex-4, derived from our friend the Gila Monster, is such a mimic and has already passed through many hoops for its diabetic uses that won't have to be repeated. Also, it readily passes the BBB and lasts several hours while GLP-1 lasts only minutes. So, we unexpectedly have a half-approved cure that really cured rats. Not only did it cure rats with PD caused by injecting one particular toxin, it also cured rats with PD caused by a second type of toxin. That is, it cured it in two unrelated models. That's good.

GLP-1 is produced in your gut when you eat and triggers insulin production in the pancreas. But its receptors are found other places including the brain. It also fits into some pretty specific spots in the PD puzzle. For example, two things that have been shown to stop PD are fasting and exercise. If you have ever fasted, after a day or so you aren't hungry. GLP-1 controls appetite. Exercise not only slows PD, it also increases production of GLP-1.

There is quite a bit more, including some white rat opportunities that increase GLP-1, but it looks better than anything that I have seen thus far.

So Merry Christmas!
__________________
Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000.
Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well.
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