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.