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Deprenyl (otherwise known as Selegiline) is currently the most promising therapy in the struggle against aging.

Recent studies have shown that Deprenyl has a variety of beneficial effects on brain aging, without producing toxic side effects.

There is much evidence to suggest that deprenyl is an antidepressant, a sexual stimulant, an effective treatment for Parkinson’s disease and a useful treatment for Alzheimer’s disease, as well as an anti-aging therapy.

Preventing and Treating Parkinson’s Disease
The most impressive clinical findings to date have been that Deprenyl slows the progression of Parkinson’s disease, and extends the life span of Parkinson’s disease patients.

In a test by Birkmayer in Austria, Parkinson’s disease patients receiving Madopar (L-Dopa plus a decarboxylase inhibitor) and deprenyl lived on average 15 months longer than patients only receiving Madopar . When 800 Parkinson’s disease patients received deprenyl in a United States and Canadian test in 1989, they were doing so much better than the control patients (who were
receiving a placebo), that the scientists directing the program halted it halfway, in order to provide the control patients with the benefits of Deprenyl. The study concluded that Deprenyl may help protect the dopamine producing neurons in the substania nigra region of the brain, from destruction. It is the loss of these neurons and the concurrent decline in the production of dopamine that causes
Parkinson’s disease. Several of the scientists experimenting with deprenyl are convinced that regular use of Deprenyl at the very early onset of Parkinson’s disease could prevent the disease entirely.

Accordingly to neurologist J William Langston of the Institute for Medical Research in San Jose, California “the evidence that Deprenyl can prevent Parkinson’s disease is strong and is getting stronger all the time”. Doctor Langston points to three compelling findings;

(A) Deprenyl is a powerful selective inhibitor of Monomine Oxidase B (MAO-B), the specific form of the enzyme that breaks dopamine into other compounds, which are then excreted. There is a marked age related rise in MAO levels, which leads to an increasing incidence of depression with advancing age. Doctor Langston also thinks that the specific type of MAO inhibition caused by Deprenyl
may also exert a protective effect on the neurons that produce dopamine.

(B) There is evidence that the dopamine producing neurons may be destroyed or made dysfunctional as a result of side effects caused by dopamine metabolism itself. Deprenyl inhibits the activity of one of the prime metabolites of dopamine called 6-OHDA, which generates oxidative free radical reactions that have been shown to have neurotoxic effects on brain neurons.

(c) Deprenyl protects dopaminergic neurons from environmental toxicity, caused by agents such as MPTP, a drug which caused severe Parkinson’s symptoms in young people who took it as a street drug in the 1970’s. It’s been shown that the toxic chemicals produced during the oxidation of MPTP destroy dopamine producing neurons and that injections of Deprenyl completely block this
destructive process.

The Unique MAO-B Inhibitor
Scientists have been exploring the use of Deprenyl as a treatment for Alzheimer’s Disease, because of its ability to inhibit the activity of MAO-B. MAO-B has been shown to oxidize the neurotransmitters dopamine, norepinephrine and phenylethylamine.

These neurotransmitters are responsible for memory,
movement, co-ordination and sex drive, and these are all functions that decline dramatically in Alzheimer patients as in Parkinson’s disease patients.

Since Deprenyl at 10mg daily has been shown to reduce the MAO-B oxidation of these neurotransmitters by 90%, it is thought that treating Alzheimer patients with Deprenyl will improve their memory and behaviour by increasing the availability of these neurotransmitters, and perhaps slow down the brain degeneration.

The earliest studies in 1987, at the Ntional Institute of Mental Health, treated 17 moderately impaired Alzheimer patients with either a placebo, or 10mg of Deprenyl daily for 28 days, or 40mg of Deprenyl for 35 days. Two patients at 40 mg daily suffered from hypertension, but there were no other serious side effects for the other patients.

The scientists concluded “significant changes for the better in behaviour, cognitive function, and neuroendocrine function compared to placebo when the patients received 10mg per day of Deprenyl, and lesser beneficial changes (with greater side effects), when the patients received 40mg per day of Deprenyl.” There were decreases in anxiety, depression, physical tension, agitation and hostility and increases in verbal communication, positive feelings about life and
greater participation in social activities.

More recent studies conducted at the Perugia University Italy treated 20 Alzheimer patients with mild to moderate Alzheimers for a 3 month period. The scientists concluded:

“Statistically significant improvements when the patients were
given Deprenyl in word fluency, digit span, long term spatial memory,
letter cancellation, picture cancellation, copy drawing, verbal memory
and concentration… Deprenyl represents an efficacious, well tolerated
and therefore reliable treatment for Alzheimer’s disease.”

Further studies at the University of Milan in 1991 with 117 patients receiving 10mg of Deprenyl or a placebo, for a 3 month period concluded:

“Deprenyl treated patients improved their performance, while
that of the placebo treated group worsened… Deprenyl seems to be an
effective treatment for patients with Alzheimer’s disease.”

Conclusions for Use in Alzheimer’s Disease
Although more research needs to be conducted to further explore the use of Deprenyl in the treatment of Alzheimer’s disease, there are some good reasons why deprenyl should be seriously considered.

(A) The findings of three controlled placebo studies, show that Deprenyl at 10mg daily is effective in improving the memory and behaviour of Alzheimer patients.

(B) The safety Deprenyl at 10mg daily has been established, with thousands of Parkinson’s disease patients who have been taking the drug for years.

(C) That Alzheimer patients are likely to benefit from the anti- Parkinson disease and anti-aging benefits of Deprenyl.

(D) That Deprenyl in combination with other drugs andsupplements provides synergistic effects (improved benefits) and maybe more effective in improving memory in Alzheimer patients than any other therapy currently available.

Slowing the Aging Process
Parkinson’s disease seems to be a form of accelerated aging, caused by the action of 6-OHDA. All elderly people suffer from symptoms of Parkinson’s disease, such as loss of co-ordination, shuffling and diminution of sex drive. This is because the exact same neurons that are destroyed in Parkinsons disease are also the same destroyed in normal aging, they just diminish at a slower rate. It is not until 80% of these neurons have diminished that the symptoms of
Parkinson’s disease are generally diagnosed.

The findings suggest that long term usage of deprenyl can slow down the aging process itself, a conclusion arrived at over 20 years ago by the Hungarian pharmacologist Joseph Knoll, who developed Deprenyl in 1965.
Figure above shows the age related decline of dopamine at 12% per decade past the age of 40, (Dean, Fowkes and Morgenthaler). Doctor Knoll’s study included 24 month old rats (65 years in human terms). They were given injections 3 times a week of a 0.25mg/ kg of Deprenyl, whilst the control animals received saline injections. The injections were continued until the animals died.
The degree of life span reported by Doctor Knoll is unprecedented for a clinically available therapy. The rats lived to an age equivalent in human terms of 150 years! It appears that deprenyl therapy slows down aging in a dramatic
fashion. Such an increase in life span could be the most important break
through in the history of medicine. Doctor Knoll’s efforts could have been simply dismissed out of hand, were it not for further evidence. More recent studies have been under taken by the Univeristy of Toronto Scientists at the University of Toronto in 1989, tried to duplicate Doctor Knoll’s efforts in another strain of rats. In the first experiment, 62 animals, 24 to 25 months of age were assigned to random groups, with the animals receiving 3 injections each week of a solution of 0.25% Deprenyl. The remainder of the animals received saline injections.

Results of the Study
The major findings of the study was that the Deprenyl group survived significantly longer than the control group. The average survival time of the Deprenyl group was 133.7 days and the average survival time of the control group was 114.7 days. The average maximum survival time of the Deprenyl group was 248.4 days compared to 212.1 days in the control group.

One animal in the deprenyl group survived 315 days and the longest span for the control group was 251 days. During autopsies no specific factors were attributable to death.

The conclusion of the study was that Deprenyl delayed the
aging of organs and that the Deprenyl treated animals were healthier
than the control animals.

Although the Toronto study produced a smaller increase in the life span of Deprenyl treated animals, than doctor Knoll’s, there were a number of other factors, which included the types, ages and weights of rats that were different between the two studies. The Toronto scientists accepted the validity of Doctor Knoll’s findings.

Doctor Knoll is now 75 years old and he takes Deprenyl
regularly and recommends that anyone over the age of 45 take it. As
he points out, the brains output of dopamine declines 13% per decade
after the age of 45 and Deprenyl is needed to protect the brains
dopamine producing brain cells from destruction.

Dosages and Side Effects
Doctor Knoll recommends taking 1 (5mg) tablet of Deprenyl three times a week. Some life extensionists recommend taking 5mg of Deprenyl daily, with an occasional break. It should be noted that no one except those suffering from Parkinson’s disease should exceed these dosage levels.

For treatment of Parkinson’s disease and Alzheimer’s diseae, the dosage of 10mg daily appears to be not only the most effective level, but also the most side effect free level. There is evidence that Deprenyl is less effective and can produce undesirable eside effects at higher dosages. But Deprenyl is remarkably safe and effective at lower dosages. Trade names include Eldepryl , Selegiline and Jumex.

The very latest evidence about Deprenyl use as a longevity/anti-aging product, is to maintain “recommended” dosages for a few months and then to reduce those dosages to approximately one third to one half.

Animal experiments show us that it is those who take low regular dosages of Deprenyl that are likely to live longer than those who take higher dosages of Deprenyl over the same period. As a result an easy to use low dosage is favourable in such circumstances.

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(1) Birkmayer J: “Neurol Transmisson” 64 113-127 1985
(2) “New England Journal of Medicine” 321 1364-1371 1989.
(3) Langston W: “Science” 245 519 1989.
(4) University of Toronto “Life Sciences” 47 415-420 1990.
(1) “Progress in Neuro psychopharmacology. Biology and
Psychiatry” 10; 537-540 1982.
(2) “Archives of General Psychiatry” vol 44 427-433 May 1987.
(3) “Clinical Neuropharmacology” Vol 13 No2 157-163 1990.
(4) “European Neurology” 31 100-107 1991.
(5) Dean W, “Multi functional deprenyl” anti-Aging Bulletin,
Volume 3 issue 1, March 1997, International Anti-Aging
(6) Knoll J, “Deprenyl and related substances, a strategy to slow
aging of the mammalian brain.” 1st Monte Carlo anti-Aging

conference, June 2000.

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