Deprenyl

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Scientific evidence from laboratories around the world suggests that deprenyl, also known as selegiline, may have broad anti-aging benefits, both mental and physical. Among other things, this compound inhibits monoamine oxidase-B, a natural substance which at increased levels has been associated with brain aging, senescence and Alzheimer’s disease. Long known as an antidepressant (although its role in alleviating depression is controversial), deprenyl has recently come into its own as an adjunct to L-dopa treatment for Parkinson’s disease. There are even impressive hints from animal studies that deprenyl lengthens life.

In 1988 Joseph Knoll, M.D., of Semmelweis University of Medicine in Budapest found that the average life span of rats treated with deprenyl was 34 percent longer than that of untreated rats. He also noted that while untreated rats lost their sexual vitality with age, 64 of 66 of the deprenyl-treated animals retained sexual vigor. More recently, in 1991, a team from the Israeli Institute for Biological Research in Ness-Ziona, reported that deprenyl significantly improved learning and memory in elderly rats.

Although deprenyl’s effectiveness as an antidepressant remains controversial, a 1988 study by J. John Mann, M.D., of the University of Pittsburgh Medical School, reported in our earlier article, concluded that deprenyl was three times better than placebo in alleviating depression. In a number of preliminary tests of deprenyl as a treatment for Alzheimer’s disease, patients showed some improvement in mental functioning, especially memory, verbal communication and daily-living skills.

The consensus among experts is that deprenyl is relatively free of adverse side effects. However, it can induce mild overstimulation similar to that from caffeine.

Because deprenyl is approved by the FDA for treatment of Parkinson’s disease (it is widely used for that purpose in both Europe and the US), it can be obtained with a doctor’s prescription and is thus among the more readily available of the anti-aging drugs. It may be well worth discussing with your doctor as a potential sexual invigorator or even as a general antiaging therapy.

DEPRENYL PROTECTS AGAINST DEATH OF NEURONS

Researchers have written a great about the benefits of deprenyl over the past few years, presenting evidence that deprenyl, in doses ranging from .5 mg every other day to 1.O mg per day, reverses the age-related increase in the enzyme monoamine oxidase B (MAO-B), which degrades the neurotransmitter dopamine, the loss of which dampens our mood, throttles our sex drive, and unhinges our coordination. It’s also been reported evidence that deprenyl combats the free radical mediated damage to neurons that plays an important role in pathologies associated with brain aging. But, perhaps, the most impressive evidence of deprenyl’s ability to fight brain aging is its ability to rescue dying neurons in tissue culture. This finding suggests that deprenyl can prevent the most critical event in brain aging-the death of irreplaceable neurons.

EFFECTS OF DEPRENYL ON BRAIN MICROANATOMY

A variety of degenerative changes occur in the brain’s microanatomy both in normal aging and senile dementia. A recent study at the University of La Sapienza in Rome, Italy (Mech Of Aging & Devel, 73:113126:1994) was designed to determine the effects of long-term administration of deprenyl on microanatomical changes in the aging rat brain, especially in areas of the brain involved in cognition, such and the frontal cortex and hippocampus, as well as the cerebellar cortex.

The Italian scientists used male Sprague-Dawley rats of 11 and 19 months of age. Twenty 1 9-month-old rats were randomly allotted to two groups of 10 animals each, which were injected with either 0.25 mg/kg of deprenyl or saline every other day. Another group of 11-month-old untreated rats was used to compare the effects of deprenyl in aging animals to healthy normal adult animals. Both the experimental and control groups were sacrificed at 24 months of age and their brains examined for age dependent changes.

DEPRENYL SLOWS MICROANATOMICAL BRAIN CHANGES

The scientists found that deprenyl was able to counteract, to some degree, all four of the age-dependent microanatomical changes in the rat brain examined in the study. The first is density of nerve cell profiles-a measure of the ability of the nervous system to receive, analyze, and store information-which is reduced progressively with advancing age in the rat brain. Less of a reduction in the density of nerve cell profiles was found in the rats given deprenyl, but this change was not statistically significant, except for the Purkinje neurons in the cerebellum.

The second parameter studied was the density of Nissl’s staining in the cytoplasm of pyramidal and Purkinje neurons, which is believed to be a measure of the ribonucleic acid content of nerve cells. Treatment with deprenyl restored the intensity of Nissl’s staining in nerve cell populations of the hippocampus and the cerebellar cortex in aged rats.

Third was age-dependent lipofuscin accumulation, which is believed to be a by-product of the peroxidative action of free radicals on membrane lipids. It was found that deprenyl decreased lipofuscin (aging pigment) accumulation in neurons, suggesting that it may have reduced oxidative stress on these cells.

Last was sulphide-silver staining within the hippocampus, which is related to the density of zinc-containing synaptic junctions, which are critical in learning, memory, and information processing within the brain. The administration of deprenyl countered, in part, the reduction of sulphide silver staining, which the scientists believe may be related to the improvement of cognitive function produced by deprenyl treatment in aged rats. (Pharmacol Biochem Behav, 39:297304:1 991).

These findings showing that deprenyl can slow important microanatomical changes in the aging rat brain provide further evidence to explain the ability of the drug to improve cognitive and behavioral function in both normally aging and demented humans by preventing the premature death of brain cells.

NEW STUDIES ON DEPRENYL

Every month, we see new studies on deprenyl showing it to be even more effective for aging than previously thought. Some of these new studies have duplicated the successful research conducted in Japan showing that one mechanism by which deprenyl extends lifespan is by boosting antioxidant enzyme levels of superoxide dismutase (SOD) and catalase. A new study has shown that oral doses of deprenyl given to dogs for only three weeks produced a dose-dependent increase of both SOD and catalase in the striatum, but not the hippocampus region of the brain (Life Sciences 54:201994). These results are in accordance with previously published results in rats. Endogenous antioxidant enzymes are more effective in preventing free radical damage than supplemental antioxidants.

Deprenyl is well known to boost brain levels of dopamine by inhibiting monoamine oxidase-B (MAO-B). Dopamine elevation conferred life extension benefits in an early study and is known to boost cognitive function and improve sexual performance. Raising base levels of SOD and catalase helps explain further the underlying mechanisms of deprenyl’s antiaging effects. In a study in the Feb 1994 issue of Mechanisms of Aging and Development, long term treatment with deprenyl was investigated on age dependent changes in the rat brain. Deprenyl treated rats (they were given the drug in their drinking water) were shown to have decreased levels of lipofuscin (aging pigment) in certain brain regions. Increased brain levels of lipofuscin have been linked to senile dementia in humans. The loss of density of certain neuronal fibers (especially in the hippocampus region of the brain) was reduced in animals receiving deprenyl (compared to the placebo group), which helps to explain deprenyl’s ability to improve memory in Alzheimer’s patients. Loss of neuronal fibers also occurs in “normal” aging.

Based upon recent studies suggesting the benefits of higher oral doses of deprenyl, the following are commonly used doses for deprenyl:

* Age 40-50: 5 mg of Deprenyl three to four times a week; * Age 50-60: 5 mg of Deprenyl four to six times a week; * Age 60-70: 5 mg of Deprenyl daily; * Over 70: 5 to 10 mg of Deprenyl daily.

Every decade over age 40-45 results in the death of 13% of the dopamine producing neurons in humans. If you suffer from an accelerated decline in your dopamine producing neurons, you are said to have Parkinson’s disease. Deprenyl protects against the death of dopamine producing neurons and for this reason alone, should be part of your life extension program if you are over 40 years of age.

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