Posted by Lorraine on March 15, 2001, at 20:26:26
In reply to Re: Selegilene Transdermal Patch, posted by steve on March 15, 2001, at 14:06:55
Here are some links with info for you:
http://www.smart-drugs.net/ias-deprenyl.htmhttp://www.deprenyl.net/#L-deprenyl plus L-phenylalanine in the treatment of depression
http://www.dr-bob.org/babble/19991212/msgs/17103.html
I have an article entitled "Pharmacology of selegiline" by Gerlach (1996, Neurology Vol. 47, no. 6)
The best one and most serious is the last article mentioned above. I do not have a link for it. Here's some more on point tho:
J Neural Transm Suppl 1998;52:109-23
Selegiline delays the onset of disability in de novo parkinsonian patients.
Magyar K, Szende B, Lengyel J, Tarczali J, Szatmary I
Department of Pharmacodynamics, Semmelweis University of Medicine, Budapest, Hungary.The pharmacological effects of (-)-deprenyl is multi-fold in its nature (dopamine sparing activity, neuroprotective and neuronal rescue effects), which cannot be explained solely by the irreversible MAO-B inhibitory action of the substance. Deprenyl slightly inhibits the re-uptake of noradrenaline and dopamine, but methylamphetamine, the metabolite of the inhibitor, by one order of magnitude is more potent in this respect, than the parent compound. Neither the metabolite nor (-)-deprenyl acts on the uptake of serotonin. The inhibitor has an intensive first pass metabolism after oral treatment. The in vivo pharmacokinetic studies with (-)-deprenyl, using the double labelled radioisotope technique (1.5 mg/kg; orally) in rats revealed that the molar concentration of methylamphetamine can reach the level suitable to induce a significant inhibition of amine uptake. Deprenyl, but especially methylamphetamine pre-treatment can prevent the noradrenaline release induced by the noradrenergic neurotoxin DSP-4. The uptake inhibitory effect of (-)-deprenyl and the metabolites is reversible. After repeated administration of (-)-deprenyl (1.5 mg/kg daily, for 8 days) sustained concentration of its metabolites was detected, compared to that of the acute studies. This can at least partly explain why (-)deprenyl should be administered daily to evoke therapeutic effects in Parkinson's disease. Administration of (-)-deprenyl in a low dose, following the toxic insult, can rescue the damaged neurones. The neuronal rescue effect of the drug was studied on M-1 human melanoma cells in tissue culture. The inhibitor reduced the apoptosis of serum-deprived M-1 cells, but the (+)-isomer failed to exert this effect. The (+/-)-desmethyl-deprenyl almost lacks the property to inhibit apoptosis. For neuroprotection and neuronal rescue an optimal dose of (-)-deprenyl should be administered, because to reach a well balanced concentration of the metabolites in tissues is critical.
Publication Types:
Review
Review, tutorial
PMID: 9564614, UI: 98225801
Still I agree that we are more likely to see studies about the good than the bad with drugs.
poster:Lorraine
thread:56167
URL: http://www.dr-bob.org/babble/20010310/msgs/56611.html