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Re: What to do if Nardil and Parnate were discontinued » ed_uk

Posted by zeugma on January 2, 2006, at 14:58:55

In reply to Re: What to do if Nardil and Parnate were discontinued » Chairman_MAO, posted by ed_uk on January 2, 2006, at 12:47:50

Hi Ed,

The problem is, many people who suffer from anxiety are likely to be frightened of having a hypertensive crisis. I don't think this is unrealistic. 'Brain selective' MAOIs could offer an important medical advance.>>

As an anxious person (especially about food, becoming sick after eating, etc.) I don't think this is unrealistic either. I, personally, would be even more afraid of what the cholinomimetic component of the drug would do to me (perhaps the only thing I fear more than food-related problems are severe episodes of sleep paralysis, cataplexy, etc., which such drugs have been known to produce), but the fear of a hypertensive crisis, even if it can be easily managed, is still going to give physicians and anxious patients pause.

I posted this a long time ago, but this MAO-B inhibitor is intriguing:

ABSTRACT

Caffeine and more specific antagonists of the adenosine A2A receptor recently have been found to be neuroprotective in the MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) model of Parkinson's disease. Here we show that 8-(3-chlorostyryl)caffeine (CSC), a specific A2A antagonist closely related to caffeine, also attenuates MPTP-induced neurotoxicity. Because the neurotoxicity of MPTP relies on its oxidative metabolism to the mitochondrial toxin MPP+, we investigated the actions of CSC on striatal MPTP metabolism in vivo. CSC elevated striatal levels of MPTP but lowered levels of the oxidative intermediate MPDP+ and of MPP+, suggesting that CSC blocks the conversion of MPTP to MPDP+ in vivo. In assessing the direct effects of CSC and A2A receptors on monoamine oxidase (MAO) activity, we found that CSC potently and specifically inhibited mouse brain mitochondrial MAO-B activity in vitro with a Ki value of 100 nM, whereas caffeine and another relatively specific A2A antagonist produced little or no inhibition. The A2A receptor independence of MAO-B inhibition by CSC was further supported by the similarity of brain MAO activities derived from A2A receptor knockout and wild-type mice and was confirmed by demonstrating potent inhibition of A2A receptor knockout-derived MAO-B by CSC. Together, these data indicate that CSC possesses dual actions of MAO-B inhibition and A2A receptor antagonism, a unique combination suggesting a new class of compounds with the potential for enhanced neuroprotective properties.>>
http://www.jbc.org/cgi/content/full/277/39/36040

Perhaps this caffeine derivative combined with moclobemide? :-)

-z


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poster:zeugma thread:591969
URL: http://www.dr-bob.org/babble/20051231/msgs/594387.html