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

You got no response from the mjf institute is because low dose naltrexone has been kicking around for awhile and it wouldn't stem from an "original idea" or be considered so by one of the bloats at the head of research. These people only have their own or their cohorts interests to serve. To hell with anybody else who would dare "scale the walls" of their ivory tower ramparts.

Ashley,

I am curious about ldn for you-I know you have been taking it for awhile, and appear not to have progressed, but how do you know that? Do you mind sharing your med schedule/history with us, so we can compare? I think it's great that ldn is helping so many (not just pd-ers, but ms and crohn's disease as well), so we need to keep spreading the word.

Thanks for sharing, and for all the great info. on ldn!

where does one get naltrexone, and how much qualifies as a low dose?

also, odd that they use the word "neuroprotection" in the headline, given that a) to my knowledge, there is still no agreed upon protocol for identifying neuroprotection, and b) all that is specifically mentioned in the body of the article is long term safety and therapeutic benefit, neither of which is neuroprotection...

To answer the above questions, I have been taking 4.5mg naltrexone daily, LDN, for the past 46 months. Originally, they said I had MS 5 years ago and gave me meds for tremor which didn't work well. I began taking Sinemet, 3 tabs, about 42 months ago which confirmed PD. Over that time my meds were adjusted so I now take 1.5 Sinemet tabs and 75mcg of Mirapex (still fairly low doses and termor is gone), also several vitamins and magnesium. Do I know if LDN "works", no I don't but so far so good. I can only hope it does but the longer my PD meds stay the same the more hopeful I am. There aren't too many people taking LDN for PD so there is not much feedback on us.
To get LDN you need an Rx from a Doctor (good luck) and then the naltrexone is compounded at 4.5mg with a filler by a pharmacy. There are docs who will Rx over the phone which is what I do. I have the LDN Rx componded by Skips Pharmacy in Fl. You can also look into dextromethorphan which has been talked about on this forum. There is a lot of info on the net also.
Hope this helps. Ashley

http://www.lowdosenaltrexone.org/index.htm
http://skipspharmacy.com/