Hi

I am on requip (9mg/day). Given the recent positive results of the MAO Inhibitor Azilect (rasagiline) I am keen to try it. I know the positive results are from manufacturer's trials but frankly if there is a sniff it will help then I want to try it.

Rasagilene is generally a monotherapy in early stage PD and my neuro has advised against my request because in his view it is requip or rasagilene not both. However I am aware of at least one other person who is relatively early stage and is on both requip (10mg/day) and selegiline (another MAO Inhibitor).

Has anyone else any experience of this?
Does anyone know why my neuro advises against?
Is there any difference between selegiline and rasagiline?

Cheers
Bryn

All I know is that my neuro has recommended Azilect and I am already on Mirapex (.5 mg 4Xday - similar to Requip) and Sinemet (1.5mg 4Xday) - I've had PD about 5 years. I've been putting off Azilect as I hate to add more chemicals and I anticipate an adjustment period, but maybe it would be helpful? I don't think there is any evidence of slowing progression beyond the very early stages, but, realistically, they probably couldn't tell yet.

Sasha

We are almost 3 years post dx and started Azilect as soon as it became available in the US. My husband takes it, mirapex, and sinemet. Of these three, he likes (and I use that word in the loosest possible sense) azilect the best because it fogs his head the least, seems to level him out the most, and he does feel worse if he misses it (we once went off it and he felt liked he took a downward turn). Got back on it asap.

We have a fairly pharmacuetically-sophisticated, if not occasionally grouchy, neuro, and I think his take on meds is pretty accurate-he is massively empirical. He is skeptical Azilect is truly neuroprotective, but is willing to wait and see what the trials bear out. He did not recommend selegiline because you had to take much more to get the same effect as azilect. On the food thing, what we got from that is that you'd have to pretty much eat an entire wheel of cheese to have a problem, but everyone is different. So far we have had no problem with food and azilect.

I will throw out there that we tried taking 2mg of Azilect because we were trying to see if the additional 1mg would have a antidepressant effect. Our neuro went along with this for awhile, but the insurance company complained and made his life difficult (since he had to justify the script) and in reality, it did not seem like the higher dose had any more effect than the 1mg. So we are back to the 1mg.

The nicotine patch helps us the most with mood, FYI. I have posted about this before. Read those posts before, and if, you decide to try it.

I don't know why your neuro is against it. My neuro would like me to take Azilect along with Requip and Stalevo. I took Azilect for about 2 1/2 months. I had a bad reaction the second day when I forgot and put grated cheddar cheese on my salad. After 2 1/2 months I was tired of avoiding cheeses and I did not see the Azilect as helping at all- it was during the time I was on Azilect that my Parkinson's symptoms began on my right side after having only been on the left side previously. So, when I had my next appointment, I told the neuro I did not want to keep taking it and he said ok. However, now he asks me at every appointment if I want to try it again.

My neuro likes Azilect and I've been on it since it came to the market here. Since then I've added Requip XL and Stalevo and haven't had any drug related problems (that I know of). I missed a day or so of Azilect and I could tell a difference, so I take it and hope that the hype of neuro protective is true.

Good Luck
ScottSuff

Azilect is a nonreversible MAO-B inhibitor--because it does not affect MAO-A receptors, its use is not associated with the "dreaded cheese effect"--ie one CAN eat cheese and other foods containing tyramines without experiencing dire adverse effects (such as hyprtensive crisis). The MAO-A's were developed and used in depression, and are much earlier developed drugs.
though anyone can have an adverse reaction to any drug--thus chickory's experience.....

From wikipedia:
MAO-A inhibition reduces the breakdown of primarily serotonin, epinephrine, and norepinephrine and thus has a higher risk of serotonin syndrome and/or a hypertensive crisis. Tyramine is broken down by MAO-A, therefore inhibiting its action may result in excessive build-up of it, so diet must be monitored for tyramine intake.

MAO-B inhibition reduces the breakdown mainly of dopamine and phenethylamine so there are no dietary restrictions associated with this. Two such drugs, selegiline and rasagiline have been approved by the FDA without dietary restrictions, except in high dosage treatment where they lose their selectivity.[1][3]



The following is from a site attributed to the primary researcher/developer of rasagiline/Azilect: Youdim MB. Note his comment that rasagiline/azilect DOES NOT have sympathomimetic activity--the activity responsible for the "dreaded cheese effect" of hypertensive crisis; thus there is no reason for restriction of tyramine containing foods one does need if using the MAO-A inhibitors used in depression. Also note the comment that azilect is "effective as monotherapy or adjunct to levodopa for patients with early and late PD-
Also reported: the theory that the propargylamine moiety is responsible for Azilect's neuroprotective effect--not its ability to decrease breakdown of dopamine. At the World Parkinson's Conference several yrs ago, this researcher maintained that in order to effectively decrease dopamine breakdown in the brain one needs to inhibit both MAO-A and MAO_B--that the real effect of azilect was from propargylamine.
http://www.rasagiline.com/neuroprotective.html

In addition, (azilect) it does not have sympathomimetic activity. Rasagiline is effective as monotherapy or adjunct to levodopa for patients with early and late Parkinson's disease (PD) and adverse events do not occur with greater frequency in subjects receiving rasagiline than in those on placebo. Phase III controlled studies indicate that it might have a disease-modifying effect in PD that may be related to its neuroprotective activity. Its S isomer, TVP1022, is more than 1,000 times less potent as an MAO inhibitor. Both drugs, however, have neuroprotective activity in neuronal cell cultures in response to various neurotoxins, and in vivo in response to global ischemia, neurotrauma, head injury, anoxia, etc., indicating that MAO inhibition is not a prerequisite for neuroprotection. Their neuroprotective effect has been demonstrated to be associated directly with the propargylamine moiety, which protects mitochondrial viability and MTPp by activating Bcl-2 and protein kinase C (PKC) and by downregulating the proapoptotic FAS and Bax protein families. Rasagiline and its derivatives also process amyloid precursor protein (APP) to the neuroprotective, neurotrophic, soluble APP alpha (sAPPalpha) by PKC- and MAP kinase-dependent activation of alpha-secretase.

Thanks to everyone for their postive responses. I shall plough on!

Bryn