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E-Newsletter No. 22

Liquid deprenyl (generic name Selegiline Hydrochloride) was developed by Professor Jozsef Knoll of Semmelweis University in Hungary. Since 1950, it has been extensively researched for treatment of Parkinson's disease and Alzheimer's disease. Recently, liquid deprenyl has been recognized as one of the most promising and safe drugs for treating Alzheimer's disease. It is found to extend maximum lifespan in animals and also acts as a cognition-enhancer in normal, healthy animals. In addition, deprenyl is found to increase sexual function in male animals and in men.


The maximum lifespan for humans under normal condition is about 110-120 years. However, the average human lives to be only 70 or 80. The maximum lifespan in rats is about 140 weeks (3years), but the average life expectancy is considerably less than that. To extend the average lifespan means to increase the number of rats living to be older than the average. As the average lifespan increased, death is postponed to later ages. The maximum lifespan does not change with increased averaged lifespan, however, there will be a greater percentage of the population approaches the maximum age. Deprenyl has been shown to extend the maximum lifespan in rats by 40%. This is the equivalent of a human living to 150 years of age. If the animal research holds true for human, a hundred-year-old would look and feel 60. In animal studies, deprenyl illustrated the effect of generalized slowing of the aging process, extended both average and maximum lifespan.


Deprenyl has become a powerful new weapon against Alzheimer's disease. In a study in Italy, 10 Alzheimer's patients were treated with 5mg of deprenyl twice a day for two months. The results showed that deprenyl improved memory, attention, and language abilities amount those who received the treatment, while those who received placebo became worse [Agnoli, et al., 1992]. Another study of 20 Alzheimer's patients treated with deprenyl also showed significant improvements in memory and attention [Peccinin,et al., 1992].

Dr. Knoll who discovered deprenyl, concluded that "Alzheimer's patients need to be treated daily with 10mg deprenyl from diagnosis until death."


In a trial study to compare the effectiveness of oxiracetam and deprenyl, 22 men and 18 women with mild to moderate Alzheimer's disease were tested. 10mg per day of deprenyl were given to one group and 800mg of oxiracetam were given to another group. The results showed that at these doses, deprenyl was more effective than oxiracetam in improving higher cognitive functions and reducing impairment in daily living. Deprenyl was found to be more effective with short and long-term memory as well as sustained concentration, attention, verbal fluency, and visuospacial abilities. Both drugs were well tolerated with few or no side effects at these doses.

Deprenyl was compared to phosphatidylserine in another study of 40 Alzheimer's patients. 10mg of deprenyl and 200mg of phosphatidylserine per day was given for three months. For most measures of cognition, deprenyl group did better.

Deprenyl was also compared to acetyl-L-carnitine (ALC) in forty patients with mild to moderate Alzheimer's disease. 10mg per day of deprenyl was found to be slightly more effective than ALC at 500mg twice daily. It is possible that the ALC dosage was too low. Nevertheless, both treatments were effective.


Deprenyl is becoming recognized as the treatment of choice for people with Parkinson's disease. Although it is well known that deprenyl dramatically slows down the progression of the disease, it is not widely recognized that deprenyl also improves cognitive function in Parkinson's disease. Several studies show that deprenyl improves attention, memory, and reaction times in Parkinson's patients. It also brings out subjective feelings of increased vitality, euphoria, and increased energy.

Deprenyl significantly delays the progression of Parkinson's disease under many conditions. Newly diagnosed patients treated with deprenyl take far longer for their symptoms to become bad enough to require L-dopa. L-dopa used to be the drug of choice for the treatment of Parkinson's disease. Many patients who are treated with deprenyl never require L-dopa. Furthermore, patients who are treated with deprenyl in combination with L-dopa live longer than those treated with L-dopa alone.


Deprenyl's chemical structure is closely related to phenylethylamine (PEA) and amphetamine. PEA is a substance found in chocolate and produced in higher than normal amounts in the brains of people who are "in love". Both PEA and amphetamine are able to cross into brain neurons and trigger the release of neurotransmitters norephrine, epinephrine and dopamine. The release of these neurotransmitters causes mental stimulation and increased alertness.

Deprenyl is unique among the PEA derivatives because it does not trigger neurotransmitter release. It is a member of a class of drug called monoamine oxidase (MAO) inhibitors. MAO is an enzyme responsible for breaking down used neurotransmitters so that they can be excreted. MAO levels tend to rise with age, and as a result, brain levels of monoamine neurotransmitters like dopamine tend to fall with age.

MAO inhibition can correct this age-related decrease in neurotransmitters. However, when MAO is over-inhibited, neurotransmitters can build up to excessive levels causing neuronal hyperstimulation-hence the "speediness" effect of amphetamines. Deprenyl manages to avoid this side effect by inhibiting only a selected form of MAO.

There are two types of MAO enzymes that are found throughout the body. Type A is found mostly in body tissue and type B is found predominantly in brain glial cells. Glial cells are small brain cells which surround and metabolically support the neurons which conduct the electrical signals through the brain.

Most MAO inhibitors are unselective, inhibiting both MAO-A and MAO-B to the similar degree. When MAO-A is inhibited with amphetamine, a dangerous high blood pressure reaction can occur in patients who eat certain foods like aged cheeses, chianti wines and chicken liver pate, which contain a chemical called tyramine. Tyramine is usually metabolized by MAO, therefore, the MAO-inhibitors causes accumulation of tyramine. This same high blood pressure reaction can occur in patients taking L-dopa for Parkinson's disease. Unlike other MAO inhibitors, deprenyl inhibits only MAO-B which does not cause the "aged cheese reaction" and it can be safely administered with L-dopa.


Deprenyl is the only drug known to selectively enhance the activity of a tiny region of the brain called the substantia nigra. Substantia nigra is exceptionally rich in dopaminergic (dopamine-using) neurons. Dopamine is the neurotransmitter that regulates such primitive functions as motor control and sex drive. Deficiencies in dopamine result in Parkinson's disease symptoms.

Degeneration of the neurons in the substantia nigra is implicated not only in the development of Parkinson's disease, but also in the aging process itself. Deprenyl protects against age-related degeneration of the substantia nigra and dopaminergic nervous system. It also protects sensitive dopamin-containing neurons from age-associated increases in glial cells and the MAO-B that they contain.

Deprenyl also inhibits the degrading of neurotransmitters and boosts the release of dopamine. Dopamine is crucial to sex drive, fine motor control, immune function and motivation. The steep decline of dopamine containing neurons in the human brain after the age 45 is universal characteristic of the aging process. The substantia nigra is the region of the brain that undergoes the most rapid aging of any brain area. It is the premature aging of this region which causes Parkinson's disease. In addition, normal age-associated depletion of dopamine causes many symptoms-most notably the gradual decline of male and, possibly, female sex drive.


Dopamine neurons age at various rates throughout the lifespan in healthy individuals. Prior to age 40-45, dopamine levels remain fairly stable. Staring at age 40-45, dopamine levels decreases by about 13% per decade. When it reaches 30% of youthful levels, Parkinson's symptom results.

Those with average and slow decline of dopamine die of other causes before Parkinson's symptoms become apparent. In fact, it has been suggested that if we all lived long enough, we would all eventually develop Parkinson's disease.


Deprenyl when combined with phenylalanine treatment is found to be very effective at relieving depression. Phenylalanine is an amino acid that acts as a precursor to neurotransmitters when taken on an empty stomach along with Vitamin B6 and Vitamin C in the Perfect Balance Formula to help nerve uptake in the brain. The clinical efficacy of deprenyl (5-10mg) plus phenylalanine (250mg) per day for depression was equaled only by the electroconvulsive treatments (ECT)---without the memory- loss side effect of ECT. However, there are side effects associated with deprenyl plus phenylalanine in some people, such as sleeplessness, anxiety, and tension. These side effects could probably be eliminated by decreasing the dose of phenylalanine, or adding a serotonergic precursor like tryptophan). It is also recommended that for optimum protection against age associated mental decline or depression, that Perfect Mind Formulas I and II be included in your daily supplement regimen.

To obtain Deprenyl, Phenylalanine, Acetyl-L-Carnitine (ALC), and phosphatidylserine, Perfect Balance, Perfect Mind I, Perfect Mind II, or the Anti-Aging Kit, please click on Nutritional Supplement Order Form.


Deprenyl's low level of toxicity, few side effects, and uniquely broad spectrum of pharmacological activities make it ideal for protection against brain aging and age-related decline of the dopaminergic nervous system. Deprenyl is a drug of choice for Parkinson's disease and is currently being established as a treatment for Alzheimer's disease. Deprenyl is a preventive treatment for aging and age-related degenerative diseases in the above-45-year-old population.

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