Michael J. Fox Foundation Announces $5.6-Million Award for Phase 2 Clinical Trial Studying Neuroprotective Potential of Inosine
http://www.earthtimes.org/articles/s...s,351176.shtml
NEW YORK, April 14 /PRNewswire-USNewswire/ -- The Michael J. Fox Foundation announced a $5.6-million award to drive a Phase 2 clinical trial to investigate the potential of inosine -- a naturally occurring chemical that gives rise to urate in the body -- to slow or stop the progression of Parkinson's disease.
The work is being funded under the Foundation's LEAPS (Linked Efforts to Accelerate Parkinson's Solutions) 2007 initiative. LEAPS 2007 was funded with a lead gift from the Edmond J. Safra Foundation, one of the most steadfast supporters of The Michael J. Fox Foundation since its inception.
Urate is a natural metabolite and major antioxidant in humans. Previous studies found that healthy people with higher urate levels in the blood had a reduced risk of developing PD. More recent work, including a study published today in the journal Archives of Neurology authored by two of the principal investigators on this LEAPS award, have linked higher urate levels to a possible slower progression of the disease.
The goals of this LEAPS award are to determine the safety of using inosine to raise urate levels, and to assess optimal dosage for therapeutic effect. Ninety people recently diagnosed with Parkinson's disease will be enrolled in a randomized, double-blind clinical trial to determine whether and at what dose inosine can safely elevate levels of urate in cerebrospinal fluid. Three months after enrollment, cerebrospinal fluid will be tested for urate levels. If a tolerable dose of inosine adequately increases urate in the cerebrospinal fluid, subjects will continue on treatment for up to two years to assess long-term safety.
"This project is precisely the sort of work that The Michael J. Fox Foundation exists to identify and drive forward for patients' benefit," said Katie Hood, the Foundation's CEO. "The study is based on interesting epidemiological observations, but because inosine is a publicly available compound, no corporate entity has the financial incentive to fund clinical research to definitively assess its potential. We believe it is our obligation to the PD community to step in where other funders may be unwilling to go, and ensure that innovative approaches like this one do not stall for lack of resources."
Inosine is widely available to consumers in dietary supplement form. The researchers emphasize that people with Parkinson's should not take inosine except in the context of a closely monitored clinical trial in which potential benefits and risks are carefully balanced. The evidence to date surrounding inosine and PD does not prove a cause-effect relationship. Additionally, elevated urate levels are known to carry certain health risks, only some of which have been definitively characterized to date. Kidney stones and gout are known risks; cardiovascular disease is a possible risk. (In the clinical trial, safety measures will be in place to help avoid these conditions, and to detect and treat them should they arise.)

Does research in this thread imply being vegetarian is bad for PD while Meat is good ?? Any body has a thought on this?

- A complete and total waste of money. NOTHING significant will come from this . If i were one of the scientists who proposed funding of this grant, I would hang my head in shame. This is the kind of self-serving money grab that will only make those involved wealthy, will cause hassle and give false hope to PWP, and is just plain ludicrous. I would bet my life that this is a "garbage" grant.

why you think this particular research is crab. we read a lot of research but difficult to sort out what is what

i'm glad that you brought this out, i would never have found it because i'm not looking at this stuff any more. But when stuff like this comes to my attention, i immediately find out all i can about the subject from both objective and bias sources. First of all, and this is standard procedure, look up what inosine is, what it does biochemically, find sources which support exactly what the stated researcher has in mind. Is there a lot of prior evidence to show that inosine fits in anywhere in the so far developed theories, which would suggest that inosine does ANYTHING more than marginally slow down PD. If it looks lame, it's probably a crab, and inosine looks LAME.
Remember, the idea of such grants are to go to top scientists in the field (scientists not related by any form of "nepotistic" affinity to the grantees, who themselves are supposed to be at the top of their fields and non-biased or in any way skewed to thinking only in terms of their life's research), for PROMISING NEW IDEAS that will lay bare the etiology of PD so that real biomechanisms of DA neuron compromisation and destruction can be found to guide other researchers, "in for the kill".
When i gave this subject my best perusal, (and i am somewhat qualified as a retired senior research chemist/biochemist), hooked what i learned with what i believe i know to be true, with any anecdotal evidence, the whole thingjust looked like "someone to throw some of this pile of cash to ,to make it look like we are using up our budget. Coming from pharma lane, it smelled too me like this kind of a boondoggle. I have seen many hopeful projects get underfunded by this kind of money grab, by people who are "closer and more connected to the source of grant money.
It's my opinion, only a "gut feeling", that from reading the literature that i found, this really is a "crab".
Last of all, and perhaps most meaningless is the fact that I have been hyperuricemic (actually early onset gout), my whole life, so that a high level of serum urate didn't protect me in anyway from getting young onset PD

I have emailed the MJFF "Scientific Staff" several times to bring their attention to the work done on low doses of naltrexone (naloxone) and dextromethorphan to slow or stop PD progression by Dr. Hong and his pharmacology group at the NIH. I have never received an acknowledgment from MJFF. Is it because these two drugs are very cheap and safe, their patents have run out long ago and no major drug company wants to spend millions in trials on people to show what the NIH has shown in rodents?
Ashley

Feel free to forward the two NIH papers below to the MJFF "Scientific Staff".
Good luck!
http://www.ncbi.nlm.nih.gov/pubmed/1...?dopt=Abstract
http://www.ncbi.nlm.nih.gov/pubmed/1...?dopt=Abstract

Inosine makes a perfectly good target.

The issue is whether dietary inosine makes it into the brain - the most successful finding to date is with regards to intracerebrally administered inosine which showed it had astonishing benefits on brain rewiring.

""The significance of this study is that it shows the largest amount of rewiring after a stroke ever found in an animal model," Dr. Benowitz says. "Of course, its relevance to humans now needs to be demonstrated.""

I am one of several forum members taking DM. I use it in the same way originally recommended for naltrexone by Dr. Bihari. The work referenced by Ashleyk by Dr. Hong and the availability of DM in pediatric cough medicines without a prescription is the basis for my substituting it for LDN.
I have been taking DM (Pedia Care Long Acting; one-half to one-third tsp. every night before bed) for six years now. I was diagnosed by the head of a university neurology department in 2001, and my symptoms have progressed very little in that time. My only other meds are generic regular sinemet, 25/ 100mg and 2X generic sinemet cr 50/200, plus 100mg amantadine.
My neuro calls me his "PD poster boy".