Deprenyl - Caveat lector
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 cerebella
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
cerebella 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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