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for educational and safety purposes
class, effects, and the receptor fingerprint, side by side; add up to four, then source the whole stack
Popular head-to-heads →MAO-BIrreversible inhibition
Neuronal apoptosis signalingModulation
Monoamine oxidase B (MAO-B, MAOB)Irreversible covalent inhibitor; the propargylamine group forms an adduct with the enzyme's FAD cofactor, so activity returns only as new enzyme is synthesised (weeks), not as drug clears (plasma half-life is a few hours).
Monoamine oxidase A (MAO-A, MAOA)Weak off-target inhibitor. Selectivity for B over A is the whole safety argument for the drug; it is preserved at 0.5 to 1 mg/day but is not absolute, and is lost at higher exposures.
Striatal dopamine catabolism (downstream consequence, not a binding site)Blocking MAO-B slows the oxidative breakdown of dopamine in the basal ganglia, raising and prolonging dopamine availability. This is the accepted explanation for the symptomatic benefit and for the levodopa-sparing effect.
Mitochondrial apoptosis pathway (Bcl-2, PKC, Bax/FAS, GDNF induction)Proposed anti-apoptotic and neurotrophic actions attributed to the propargylamine moiety rather than to MAO inhibition. Preclinical only; not demonstrated in humans.
MAO-AIrreversible inhibition
checking Rasagiline and Clorgyline: at least one combination is flagged to avoid (1 to avoid). treat the red pairs as a reason to reconsider mixing.
combining two MAO inhibitors compounds the enzyme blockade; a well-known dangerous combination.
General educational info, not medical advice.