Deprenyl (selegiline), a selective MAO-B inhibitor, is known to improve motor functions in Parkinson's disease and delay the need for levodopa therapy in patients with early Parkinson's disease. It is not clear at this time whether it has longevity enhancing potential, but my educated guess would be that high doses would actually be harmful due to potential heart rhythm abnormalities. Deprenyl raises levels of dopamine. The nutrient NADH is also able to raise dopamine levels.
I have noticed that deprenyl (selegiline) provides a sense of wellbeing with slightly brighter vision and libido. High doses may induce heart palpitations or irregularities. Periods of alertness and sleepiness are possible.
Deprenyl is a prescription medicine but can be obtained from overseas.
Adverse effects include heart rhythm disturbances, sleepiness at times during the day and insomnia at night.
Due to its influence on dopamine, deprenyl can enhance sexual desire. After years of research, Dr. Sahelian has formulated Passion Rx, a highly advanced libido product for men and women that has a significant effect on libido, sensuality and stamina, erections, orgasms, energy and mood.
Interactions with dietary supplements
I understand that sam-e has some neurotransmitter effects. Would there be any adverse interactions between sam-e (at approx 1 g/ed) and deprenyl at 2.5 mg/d, or can they be taken together with no problems?
SAM-e has a stimulatory nature and even 200 mg can be a lot for some people. Deprenyl can stimulate dopamine levels, the combination may be too much and overly energizing, however if dosages are kept very low for both, it may work, under medical supervision.
Metabolism of Deprenyl
Curr Med Chem. 2013.
Used to treat patients with Parkinson's disease. Nevertheless, in much higher doses it has beneficial effects in depression, and dementia of the aged patients. It undergoes a complex metabolic pathway. Its major metabolites include desmethylselegiline, methamphetamine and (-)-amphetamine, selegiline-N-oxide and formaldehyde as a small metabolic fragment in animal experiments. In addition, more than 40 minor metabolites have also been either detected or proposed by investigators and researchers.
Eur J Pharmacol. 2015. The effect of deprenyl administration on reproductive parameters of rat males.
Pharmacological aspects of deprenyl. Current Medical Chem. 2004.
Deprenyl, the selective irreversible inhibitor of monoamine oxidase-B (MAO-B), has been synthesised as a potential antidepressant, however, due to its dopamine potentiating capacity, became a registered drug in the treatment of Parkinson's disease. Deprenyl possesses a wide range of pharmacological activities; some of them are not related to its MAO-B inhibitory potency. Beside its dopamine potentiating effect, it renders protection against a number of dopaminergic, cholinergic and noradrenergic neurotoxins with a complex mechanism of action. By inducing antioxidant enzymes and decreasing the formation of reactive oxygen species, deprenyl is able to combat an oxidative challenge implicated as a common causative factor in neurodegenerative diseases. In a dose substantially lower than required for MAO-B inhibition, deprenyl interferes with early apoptotic signalling events induced by various kinds of insults in cell cultures of neuroectodermal origin, thus protecting cells from apoptotic death. Deprenyl requires metabolic conversion to a hitherto unidentified metabolite to exert its antiapoptotic effect, which serves to protect the integrity of the mitochondrion by inducing transcriptional and translational changes. Pharmacokinetic and metabolism studies have revealed that deprenyl undergoes intensive first pass metabolism, and its major metabolites also possess pharmacological activities. The ratio of the parent compound and its metabolites reaching the systemic circulation and the brain are highly dependent on the routes of administration. Therefore, in the treatment of neurodegenerative diseases, reconsideration of the dosing schedule, by lowering the dose of deprenyl and choosing the most appropriate route of administration, would diminish undesired adverse effects, with unaltered neuroprotective potency.
l-Deprenyl prevents lipid peroxidation and memory deficits produced by cerebral ischemia in rats.
Cell Mol Neurobiol. 2004.
The present work shows the results on behavior and on biochemical parameters of l-deprenyl (0.1, 5, and 10 mg/kg, p.o.) administered daily for 5 days to rats submitted to global cerebral ischemia. The transient global ischemia was carried out by clamping the animals bilateral common carotid arteries for 20 min. The parameters studied were memory acquisition and memory retention, locomotor activity and thiobarbituric acid reactive substances, as an index of lipid peroxidation. 3. l-Deprenyl treatment significantly improved memory deficits as compared to the ischemic group as measured by the elevated T maze test. A similar result was observed on the passive avoidance test where l-deprenyl improved late but not early memory as compared to the ischemic group. Except for an increased locomotor activity observed in the group treated with 5 mg/kg, no other alteration was detected in this behavioral test. Rats submitted to transient global ischemia (and without l-deprenyl) showed an increase in MDA levels in the hippocampus and the treatment with l-deprenyl (5 or 10 mg/kg) significantly reversed this effect bringing values close to those of the sham-operated controls. A similar profile was observed with nitrite levels. 4. In conclusion, the work showed a significant protective effect of l-deprenyl on memory deficits and lipid hyperperoxidation observed after cerebral ischemia. Possibly, the drug is acting at least in part through its antioxidant activity.
Q. I am considering purchasing some of your products, one being sam-e. I understand that sam-e has some neurotransmitter effects. Would there be any adverse interactions between sam-e (approx 1 g/ed) and deprenyl at 1-2.5 mg/d, or can they be taken together with no problems?
A. SAM-e has a stimulatory nature and even 200 mg can be a lot for some people. Deprenyl can stimulate dopamine levels, the combination may be too much and overly energizing, however if dosages are kept very low for both, it may work, under medical supervision.
Q. I am trying deprenyl at 1-2.5 mg day in the morning
and I think I get the side effect you mention: "Periods of alertness and
sleepiness are possible. "Can you please point me to some resource to understand
this or give me a brief explanation?
A. I'm guessing that this may be due to the effect of dopamine on the sleep/awake centers in the brain. There are times during the day when dopamine may actually cause sleepiness, and also there are areas in the brain where dopamine would lead to sleepiness whereas other parts of the brain exposed to dopamine would cause alertness.
I have read where deprenyl is
currently being prescribed both as a preventive and as a cure for Parkinson's
Disease? Can you share what information you have regarding this drug?
This medication is helpful in some patients with PD, but it is not a cure.