Posted by undopaminergic on December 8, 2019, at 9:03:11
In reply to MAO-B elevated in Depression, posted by linkadge on December 7, 2019, at 9:17:09
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> Although MAO-B inhibitors are not effective in their own right (in many cases) as antidepressants, MAO-B appears to be elevated in major depression. Hence (perhaps) some degree of MAO-B inhibition would still prove therapeutic in patients with depression.
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> LinkadgeThat is an interesting finding. Normalising the MAO-B levels is probably a good idea. Reducing it to abnormal levels, I don't know for sure.
While taking 10 mg/day (or even more) of selegiline resulted in more of an improvement than a worsening, I don't know whether there is something subtly negative about it. It changes the way certain substances are metabolised. For example, it likely changes the role phenylethylamine (PEA) normally plays in neuromodulation (especially dopaminergic).
Also, with selegiline (l-deprenyl) there is the question of the l-amphetamine metabolites. They play a significant role in the pharmacology of the drug. The amphetamine levels produced are far too low to be neurotoxic, but they are the likely reason for the initial stimulation (including a mood lift) you experience upon initiating selegiline. I know this, because I did not experience any stimulant effect when I started rasagiline (a similar MAO-B inhibitor), which does not metabolise into amphetamines.
-undopaminergic
poster:undopaminergic
thread:1107068
URL: http://www.dr-bob.org/babble/20191019/msgs/1107094.html