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Joseph Knoll

acquisition of a drive from the start of training until its manifestation.

David: What are some of the disorders that deprenyl has proven itself to be an effective treatment for?

Dr. Knoll: Successful clinical studies with deprenyl were executed in depression and in the two age-related neurodegenerative diseases: Parkinson’s Disease and Alzhiemer’s Disease. The first clinical study performed in depressed patients by Dr. Varga with deprenyl was published in 1965. The clinical use of deprenyl in Parkinson’s Disease started in 1977. The first two papers demonstrating the effectiveness of deprenyl in Alzhiemer’s Disease appeared in 1987. Deprenyl was originally developed with the intention to be used as a new spectrum antidepressant. Its effectiveness was first demonstrated with the racemic form of the compound by Dr. Varga and his coworkers in 1965 and 1967, and with the  enantiomer in 1971. The first study that corroborated the antidepressant effect of deprenyl was published by Dr. Mann and Dr. Gershon in 1980.

The realization of the peculiar effect of deprenyl–first in Parkinson’s Disease and later in Alzhiemer’s Disease–distracted attention from its antidepressant property which remains unutilized. Even an especially interesting aspect of this problem fell into oblivion. In a depression study performed by Dr. Birkmayer and his coworkers in 1984 on a hundred and two outpatients and fifty-three inpatients, deprenyl was given together with phenylalanine. The latter is the precursor of phenylethylamine (PEA) that, in contrast to PEA, crosses the blood-brain barrier and, as it is metabolized in the brain, increases the concentration of this natural enhancer substance. Nearly seventy percent of the patients achieved full remission from depression. The outstanding clinical efficiency was equaled only with that of electroconvulsive treatment, but without the latter’s side effect of memory-loss.

David: How might healthy people utilize deprenyl for its cognitive enhancing and antiaging benefits?

Dr. Knoll: They should take one milligram of deprenyl daily from sexual maturity until death.

David: Some studies have shown that deprenyl can significantly increase the maximum life span of laboratory animals, yet some of the longevity researchers that I’ve spoken with told me that these findings have been difficult to replicate. Why do you think this is, and what are your thoughts about this?

Dr. Knoll: Our finding that deprenyl prolongs life was corroborated in mice, in rats, in hamsters, and in dogs. Nevertheless, variation in the extent of the prolongation of life between the longevity studies performed in different laboratories was unusually high. The reason for this variation is now clear. A bell-shaped concentration effect curve is characteristic to the enhancer effect of the synthetic mesencephalic enhancer substances. Thus, there is an optimum dose for the enhancer effect.

Concerning the optimum dose of deprenyl there are, not only species, but also strain differences. On the other hand , even the effect of an optimum dose depends on the selected experimental conditions. We worked, for example, with the long-lived, robust, Wistar-Logan strain, which seldom grows tumors. The age of rats at the start of treatment was two years in our first study and roughly eight months in our second study. In both studies a substantial number of rats treated with deprenyl lived longer than the estimated technical life span of three and a half years.

Dr. Milgram and colleagues were the first who repeated our survival study with deprenyl. They clearly intended to hold tightly to the parameters we used in our first study, and started experiments with two year old rats and treated them with 0.25 milligrams per kilogram with deprenyl. They changed, however, an important parameter. They worked with the short-lived Fischer 344 strain of rats, thus, they started treatment too late and found only a sixteen percent marginally significant prolongation of life span. Nevertheless, they found a convincingly significant increase in the longer survival.

Dr. Kitani and colleagues, who conducted the second control survival study with deprenyl, also used Fischer 344 rats. They obviously considered that these rats are shorter living than the Wistar-Logan rats, and they started to work with one and a half year old rats. This was an advantageous change in the experimental conditions and found a satisfyingly significant, thirty-four percent prolongation of the average life span.

However, in the hope to increase the effectiveness of their treatment they doubled the dose of deprenyl. Although a higher dose is usually more effective than a lower one, the doubling of the dose was in this special case an unfavorable change. We know now that 0.01 milligrams per kilogram of deprenyl is sufficient to exert an enhancer effect. Thus the 0.5 milligrams per kilogram dose was obviously enormously high, and this explains why Kitani and colleagues found no sign of the significant extension in the longest survival which appeared in our studies and in the Milgram et al. study.
All in all, in future longevity studies with a synthetic mesencephalic enhancer substance, it is reasonable to treat the animals with a dose that in preliminary studies proved to exert a peak effect in enhancing the release of catecholamines and serotonin in the brain stem.

David: What do you think are the primary causes of aging in general?

Dr. Knoll: Various species live together on earth in a harmonious proportion. This is obviously carefully regulated. One of the seemingly principal regulatory mechanisms that produces equilibrium among living organisms is brain aging. It ultimately leads to the elimination of those individuals who have already fulfilled their duty in nurturing the new generation.

Accordingly, the period from weaning until sexual maturity is reached is the most delightful phase of life, the glorious uphill journey. The individual progressively takes possession, on a mature level, of all abilities crucial for survival and maintenance of the species. It learns to avoid dangerous situations, masters the techniques to obtain its food, develops procreative powers for sexual reproduction and copulates. This is, at the same time, the climax of developmental longevity. The sexually fully mature individual fulfils its duty. Thus, to maintain the precisely balanced out natural equilibrium among living organisms, the biologically “useless” individual has to be eliminated. According to the inborn program, the postdevelopmental stage of life (aging) begins. The essence of this stage is progressive decay of the efficiency of the catecholaminergic system during the postdevelopmental life span until at some point, in an emergency situation, the integration of the parts in a highly sophisticated entity can no longer be maintained and “natural death”, signaled by the disappearance of the EEG signal, sets in.

David: What do you think are currently the best ways to slow down, or reverse, the aging process and extend the human life span?

Dr. Knoll: Regarding the quality and duration of life the most important aging process is the continuous, slow, age-related decline of the mesencephalic enhancer regulation during the postdevelopment phase of life. This can not be reversed, but its progress can be slowed by the prophylactic administration of a synthetic mesencephalic enhancer substance (for the time being with the daily administration of one milligram of deprenyl). The earlier this protective treatment starts, the better are the prospects to improve the quality of life in the latter decades, which necessarily goes together with an extension of life span.

David: How long do you think it’s possible for the human life span to be extended?

Dr. Knoll: The average life span in the most developed countries has already exceeded the eighty year level. This change has come about due to the prevention of premature deaths owing to the development of hygiene, immunology, and chemotherapy. The human technical life span (TLSh), close to a hundred and twenty years, has remained, however, unchanged.
In my view, to extend the human life span beyond the TLSh needs the elaboration of an ultimate technique for the prophylactic, daily small-dose administration of a safe synthetic mesencephalic enhancer substance from sexual maturity until death. The attainable upper limit in the extension of the TLSh is obviously unpredictable at present. Nevertheless, if brain research could, at some time in the future, achieve just a doubling of the TLSh, this will mean for humans the most significant accomplishment that science has ever achieved, since nothing can be more important for the individual than the quality and duration of his/her life.

David: What are some of the new anti-aging treatments that you foresee coming along in the near future?

Dr. Knoll: In the developed countries the proportion of the aged is high, and the estimated number of individuals over sixty-five will increase to 1.1 billion by 2050. Accordingly, the demand on antiaging therapy is rapidly increasing. This trend explains the already high-sounding proposals for antiaging treatments.

My view is that since the brain alone ensures that the mammalian organism works as a purposeful, motivated, goal-directed entity, the age-related changes in the central nervous system are of particular importance. And since the enhancer-sensitive neurons in the brain stem work as the engine of the brain, the slow, continuous, postdevelopmental functional decline of the mesencephalic enhancer regulation is of primary importance in the maintenance of the well-balanced equilibrium

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