 Mono-Amine Oxidase (MAO) is the enzyme which breaks down inactive neurotransmitters in the brain. There are two forms, A and B, the "A" form, MAO-A, breaks down the neurotransmitters serotonin, adrenalin and nor-adrenalin. MAO-B breaks down the neurotransmitter dopamine. MAO-A inhibiting drugs are used as anti-depressants, whereas drugs that inhibit MAO-B are used as treatments neurological degenerative diseases like Parkinson's Disease. Reduction in the breakdown of the neurotransmitters serotonin, adrenalin & noradrenalin with MAO-A inhibition reduces depression, but unfortunately elevates blood pressure. Deprenyl also was originally used as anti-depressant because it inhibited both MAO-A and MAO-B in dosages above 30-40 mg per day. It was soon discovered that deprenyl's selective inhibition of MAO-B at dosages below 20 mg/day made it a useful in the treatment of chronic dopamine depletion ailments like Parkinson's Disease and with no blood-pressure elevation problems.  Deprenyl has been shown to play a positive role on the immune system as well as its neurodegenerative effects. Deprenyl offers protection against DNA damage and oxidative stress and against excitotoxic damage from glutamate. In addition, deprenyl stimulates the release of superoxide dismutase or SOD, which is a key enzyme that helps to suppress the production of destructive free radicals. Due to Deprenyl’s ability to permeate the mitochondria’s membranes it actually protects the mitochondria. Mitochondria are the energy powerhouses of the body’s cells where oxygen respiration occurs. A popular theory of aging suggests one cause of aging is free radical damage to mitochondrial DNA.  Deprenyl was discovered around in 1965 in Hungary by Dr. Joseph Knoll and colleagues. It is a drug that has been intensively researched over the past 40 years and many hundreds of research papers on Deprenyl have been published. According to Dr Knoll Deprenyl is an exceptionally lucky modification of phenylethylamine a member of the noradrenaline and dopamine family. It had shown to have a unique and exciting pharmacological profile by being the only potent selective MAO-B inhibitor in medical use. Deprenyl also protects nerve cells against a wide number of neurotoxins. To list some of Deprenyl’s uses and merits, it has in some instances become a standard treatment for Parkinson’s disease and become a useful treatment for drug-resistant depression. Its function shows much promise as a cognitive enhancer and in four different rat studies and one dog study to be an effective life-extension agent. Another benefit was the increase in sexual behaviour in aged rats. During the 1990s Knoll’s Deprenyl research took a new direction, he discovered a new mode of action of deprenyl that he believes explains its widespread clinical utility. Knoll discovered that Deprenyl is a catecholamine activity enhancer. Catecholamines are the inter-related neurotransmitters dopamine (DA), noradrenalin (NA) and adrenalin. Catecholamines are the transmitters which activate brain circuits responsible for focus and concentration for example .It is dopamine that helps control bodily movements which partially die off and malfunction in Parkinson’s disease. Deprenyl creates a greater release of transmitters in reaction to an electrical impulse which increases Catecholamine nerve cell activity. Of course this may be clinically very useful in Parkinson’s disease and Alzheimer’s disease, where circuits under-function. Knoll’s research also indicates that after sexual maturity the activity of the Catecholamine nervous system gradually declines, and that the rate of decline determines the rate at which a person or animal ages. He believes that Deprenyl’s Catacholine enhancing effect explains its anti-aging benefit. Parkinson’s disease (PD) is one of the two largest neurodegenerative diseases of the modern world - Alzheimer’s disease is the other. PD affects up to 1% of those over 70, a lesser percent of those 40-70, and rarely anyone below 40. PD is caused by a severe loss of dopamine neurons, with symptoms manifesting after 70% neuronal loss, and death usually ensuing after 90% loss. In 1985 Birkmayer, Knoll and colleagues published a paper concluding the results of 9 years of treatment with L-dopa alone or combined with Deprenyl in PD. They found a typical 1 to 2 year life extension over the average 10 years from L-dopa alone until death in the L-Dopa/Deprenyl group. In a 1992 paper Lieberman supporting the claim that in L-dopa treated patients with moderate or advanced PD the addition of Deprenyl is beneficial. By the 80s/90s Deprenyl had become the standard PD therapy, used either to delay L-dopa use, or in combination with L-dopa. Alzheimer’s disease (AD) is the most widespread neurodenerative disease affecting several millions worldwide. AD is characterized by severe memory loss, verbal dysfunction, learning disability and personality disorders. The deterioration in dopamine and to the noradrenergic systems appear to cause cognitive disorders like memory and attention deficits. AD sufferers show increased MAO-Bs therefore it makes sense to inhibit MAO-B’s to improve cognitive function. One such study in fact concluded “Deprenyl is useful as initial therapy in patients with mild-to-moderate Alzheimer disease to manage cognitive behavioural symptoms. In patients with moderate-to-severe Alzheimer disease and it should be considered among the various treatment options”. After nearly 50 years of research, Dr Knoll has concluded that “...the regulation of lifespan must be located in the brain, and catecholamine nerve activity reaches a maximum at sexual maturity, and then begins a long, gradual downhill slide thereafter. Animal research has shown catecholamine activity, learning ability, sexual activity and longevity to be inextricably interlinked.” He argues that a high performing longer living individual has a more active, more slowly deteriorating catecholamine system than [his/her] low performing, shorter living peer.” From the point of view from the active life extension enthusiast Dr Knolls most exciting conclusion was that “...the activity of the catecholamine system can be improved at any time during life, it must be essentially feasible to ... [transform] a lower performing, shorter living individual to a better performing, longer living one.” In other words you have the power to change something which seems to be your destiny or your fate which you may believe to be in the lap of the Gods. For the last 30 years people have been asking if this wonderful drug is in fact the elixir of life itself. This is not for us to comment but the thousands of clinical studies and papers written on Deprenyl demonstrate its many wonderful actions against the deteriorating brain. It is on this basis that Dr Knoll consistently recommends the use of 10 - 15 mg oral Deprenyl per week, starting in the 40s, to help achieve this goal in humans. Knoll’s research clearly convinces him that deprenyl is both a safe and effective catecholamine activity enhancer and MAO-B inhibitor. DEPRENYL: DOSAGE & SIDE-EFFECTS Both Dr. Joseph Knoll and the Life Extension Foundation recommend a 10-15 mg weekly (i.e. 1.5 - 2 mg/day) oral Deprenyl dosage for humans, starting around age 40, possibly even in the 30s. 10 mg/day is a relatively standard dose for treatment of PD and AD, but this higher dose should only be used with medical supervision. Some experts believe this dosage is excessive, and that with long term use lower doses may still be effective and safer. Knoll has noted that the human MAO-B inhibiting dose ranges from 0.05 to 0.20 mg/kg of bodyweight. Thus, even in those wishing to use it at an effective MAO-B inhibiting dose, it should not be necessary to use more than 3-5 mg/day. Because Deprenyl is a potent and irreversible MAO-B inhibitor, it may even turn out in many individuals that the suggested 1.5-2 mg/day “life extension” dose may achieve MAO-B inhibition with long term use. Deprenyl is reported in most human studies to be well tolerated. Typically, no abnormalities are noted in blood pressure, laboratory valves, ECG or EEG. The most common side effects reported are gastrointestinal symptoms, such as nausea, heartburn or upset stomach. Some studies have found side effects such as irritability, hyper-excitability, psychomotor agitation and insomnia. These effects are probably due to over-activating the DA/NA neural systems at the expense of calming/sleep-inducing serotonin systems, so taking magnesium and tryptophan or 5-HTP may suffice to counter these “psychic” effects. As with all medications, please consult your doctor or pharmacist. Deprenyl is presently being tested on the affects of over-use of the drug MDMA or ecstacy because of the excessive dopamine production leading to the depletion of the serotonin system. It is also being tested as a drug to combat the addictive qualities of tobacco. The FDA are also considering the administration of deprenyl via a patch for major depression, this should be available this year 2005 and if agreed it will be the first transdermal treatment for major depression. Deprenyl was developed in the 1960’s as a brain energiser and antidepressant. Later it was administered with other agents for Parkinson’s Disease. A huge amount of research has shown Deprenyl to be a safe multi faceted drug. Deprenyl improves the availability of dopamine and slows age related mental decline by acting as a selective MAO-B inhibitor. MAO is a neurotransmitter (a chemical messenger carrying impulses to nerve cells) which generally rises with age which in part causes dopamine decline. In fact human longevity is partly governed by the rate of dopamine decline. Starting at age 45 dopamine levels in healthy individuals begin to decrease at a rate of approximately 13% per decade. When dopamine levels reach approximately 30% of ‘normal’, Parkinson’s symptoms begin to show. 10% of the ‘normal’ levels equals death.
Deprenyl improves brain function/ slows age decline/ has anti depression properties and in men can help improve sexual function and desire. It has been described as a safe agent that enhances both the quality and length of life.
Deprenyl comes as a liquid or in tablet form. The liquid has the easy dosage system of each 1ml drop being equivalent to 1mg of deprenyl citrate.
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