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Jumex Review Article

 

DopamineJumex (Selegiline), also known as Deprenyl, Eldepryl works by helping to conserve the amount of dopamine available by preventing the dopamine from being destroyed. While controversial, there is some evidence that this drug may slow the progression of Parkinson's disease, particularly early in the course of the disease. Jumex works by helping to conserve the amount of dopamine available by preventing the dopamine from being destroyed. While controversial, there is some evidence that this drug may slow the progression of Parkinson's disease, particularly early in the course of the disease. This drug is well-tolerated by most people, so many experts recommend using it despite the controversies.
Indications Jumex (also known as Deprenyl, Selegiline, Emsam, Zelapar or Eldepryl) is approved for treatment of Parkinson’s disease in Europe and United States. Furthermore research findings based on animal and human experiments have shown that there is a possibility of Jumex acting as an anti-ager both in delaying the onset of age related deterioration in the functioning of the brain and in the improvement/ maintenance of sexual vigor. Jumex also has the advantage of being potent and highly selective. In fact it is the only clinically available MAO-B inhibitor. Continue reading...

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Jumex is used to treat Parkinson's disease. Parkinson's disease is associated with low levels of a chemical called dopamine (doe PA meen) in your brain. The exact way that eldepryl works is unknown. However, it is believed that eldepryl prevents the breakdown of dopamine in your brain. Eldepryl is usually added to a treatment regimen after levodopa / carbidopa therapy begins to deteriorate. Jumex is also used to treat the stiffness, tremors, spasms, and poor muscle control of Parkinson's disease. It is also used to treat the same muscular conditions when they are caused by drugs such as chlorpromazine (Thorazine), fluphenazine (Prolixin), perphenazine (Trilafon), and others.

Background of the disease which Jumex treats
Jumex was discovered over 4 decades ago in Hungary at the University of Semmelweis in Budapest by Joseph Knoll. Jumex has since then been used widely in the treatment of Parkinson’s disease. Parkinson’s disease sets off as a result of degeneration of the dopamine levels in the brain (Knoll, 1992) and this is usually associated with aging. The rate of decrease of dopamine level after the age of 45 is thought to increase at an average rate of 13% every decade (Knoll, 1989; Magyar, 2004). Symptoms of Parkinson’s disease begin to take effect when the level drops to 30%. Under normal circumstance the dopamine level does not reach this stage throughout an individual’s lifespan but in the case of increased deterioration, Parkinson’s disease will develop in old age. A drop in dopamine levels in the brain below 10% of the original results in death of the individual. Therefore treatment of Parkinson’s disease is important in the prevention of premature death and improvement of quality of life in the elderly.

Mechanism of action:

Jumex acts as a selective monoamine oxidase (MAO-B) inhibitor (Magyar and Szende, 2004). It competes with MAO-B to metabolize dopamine and phenylethylamine. The production of MAO-B is associated with the deteriorated functioning of the dopaminergic nervous system. The drug is the first selective MAO-B inhibiting drug that has been widely used in the treatment of Parkinson’s disease. Unlike other MAO deprenyl has the advantage of not requiring a restricted diet as it follows a mechanism which does not interfere in this process.

Jumex provides selective protection against the age-related degeneration of the dopaminergic nervous system. It protects sensitive dopamine-containing neurons from the age-associated increases in glial cells (non-neuron brain cells) and the monoamine oxidase (type B) that they contain. Jumex is the first selective inhibitor of MAO-B ever discovered, it is the only one used in clinical practice, and it remains the scientific reference standard for B-type inhibition after more than 40 years.

Jumex also competitively inhibits the uptake of dopamine, norepinephrine and epinephrine (collectively referred to as catecholamines) into neurons. This unique ability among the MAO inhibitors prevents the “cheese effect,” a dangerous hypertensive reaction caused by neural uptake of tyramine from tyramine-containing foods like aged cheeses, certain wines, yeast, beans, chicken liver and herring. Eldepryl exhibits no significant cheese effect at therapeutic dosages, and only minimal effects at extremely high dosages.

Jumex is a drug that was discovered around 1964-65. It was originally developed as a “psychic energizer,” designed to integrate some amphetamine-like brain effects with antidepressant effects. Also known as L-deprenyl, (-)-deprenyl, and selegiline, eldepryl has been intensively researched over the past 36 years - many hundreds of research papers on eldepryl have been published. Eldepryl has been shown to protect nerve cells against a wide (and growing) number of neurotoxins. Eldepryl has also been shown to be a “neuroprotection/ neurorescue agent” when nerve cells are exposed to damaging or stressful conditions.

Clinical Trials

Several clinical trials on human subjects have shown dopamine to delay the onset of symptoms and increase the survival rate of patients with Parkinsons diseases especially when diagnosed early (Knoll et al, 1983). Although the use of Jumex as a general anti-aging drug when used on a long term basis is yet to be directly tested on humans, extensive studies on animal models suggest a great possibility of Jumex as an anti-ager (Knoll et al, 1988; Milgram et al, 1990; Kunikowska et al, 2002). It has also been found that Jumex has an effect of delaying the onset of increased hunger sensation related to aging (Zeng et al, 1994). Furthermore the significance of Jumex in the treatment of Alzheimer’s disease is also being extensively researched (Tariot et al, 1987; Guly?s et al, 2011). Some studies have also observed a relationship between deprenyl use and improved sexual performance in male rats (Melis and Argiolas, 2000) As more research findings are revealed on this drug it has a promising prospect as a good choice for both treatment of age related diseases such as Parkinson’s disease and Alzheimer’s disease as well as being used on a long term as an anti-aging strategy. More recently Jumex is being studied as a possible candidate to assist people to quit smoking (Weinberger et al, 2010). Tests on nicotine dependent adult smokers indicated Jumex to be a safe drug to be taken by smokers however the results are not conclusive enough to suggest a strong relationship between Jumex and smoking cessation.

Dosage Form:

Jumex is often used in combination with other anti-Parkinson’s disease drugs such as levodopa for more effective treatment. The dosage level is prescribed by the doctor based on the specific patients requirement. It is often available in the oral form to be swallowed with water with or without meals. It is also available as a transdermal patch (Fang et al, 2009) which is to be placed on top of the skin after which the drug is absorbed at a controlled rate into the body.

The dose of Jumex will be different for different patients. Your doctor will determine the proper dose of eldepryl for you. Follow your doctor's orders or the directions on the label.

For the treatment of Parkinson's disease, the usual dose of eldepryl is 5 mg two times a day, taken with breakfast and lunch. Some patients may need less than this.

Dietary and Alcohol Considerations:
Alcoholic beverages or alcohol-free or reduced-alcohol beer and wine.
Foods that have a high tyramine content (most common in foods that are aged or fermented to increase their flavor), such as cheeses; fava or broad bean pods; yeast or meat extracts; smoked or pickled meat, poultry, or fish; fermented sausage (bologna, pepperoni, salami, summer sausage) or other fermented meat; sauerkraut; or any overripe fruit. If a list of these foods and beverages is not given

Storage:
Keep this medication in the container it came in, tightly closed, and out of reach of children. Eldepryl should be stored at below 30°C (86°F) and away from excess heat and moisture (not in the bathroom). Heat or moisture may cause the medicine to break down. Keep away from light. Talk to your pharmacist about the proper disposal of your medication. Throw away any medication that is outdated or no longer needed. Be sure that any discarded medicine is out of the reach of children.

Package Size and Type:
Tablets: 5 mg, 10 mg.

Caution! Before starting to take this medicine, it is vital that you should consult your doctor! Do not use it on your own initiative, without medical advice.

References
Fang Jia-You, Chi-Feng Hung, Chen-Hsien Chi, Chih-Chieh Chen. Transdermal permeation of selegiline from hydrogel-membrane drug delivery systems. International Journal of Pharmaceutics, 380(1-2): 33-39, 2009.

Guly?s Bal?zs, Elena Pavlova, P?ter K?sa, K?roly Gulya, Lidia Bakota, Szilvia V?rszegi, ?va Keller, M?nika Csilla Horv?th, Sangram Nag, Istv?n Hermecz, K?lm?n Magyar, Christer Halldin. Activated MAO-B in the brain of Alzheimer patients, demonstrated by [11C]-L- deprenyl using whole hemisphere autoradiography. Neurochemistry International, 58(1): 60-68. 2011.

Kazuhiro Nakaso, Chiharu Nakamura, Hiromi Sato, Keiko Imamura, Takao Takeshima, Kenji Nakashima. Novel cytoprotective mechanism of anti-parkinsonian drug deprenyl: PI3K and Nrf2-derived induction of antioxidative proteins.
Biochemical and Biophysical Research Communications, 339(3): 915-922. 2006.

Knoll J, Extension of life span of rats by long-term (-)deprenyl treatment. Mount Sinai J Med 55: 67-74, 1988.
Knoll, J. "Deprenyl (selegiline): The History of Its Development and Pharmacological Action" Acta. Neurol. Scand. Supp.95:1983. pp. 57-80.
Knoll, J. "Deprenyl Medication: A Strategy To Modulate the Age-Related Decline of the Striatal Dopaminergic System" Journal of the American Geriatric Society. V.40., No.8, August, 1992, pp. 839-847.
Knoll, J. "The Pharmacology of Selegiline ((-)Deprenyl): New Aspects" Acta Neurol. Scand. 1989:126 pp. 83-91.
Kunikowska, G., Gallagher, I., Glover, V., Clow,A., Jenner, P. Effects of short and long term (-) deprenyl administration on mRNA for copper, zinc and manganese-superoxide dismutase and glutaminhione peroxidase in rat brain. Brain Research. 953(1-2). 2002.
Magyar and Szende, (-) Deprenyl, A selective MAO-B inhibitor, with Apoptotic and Anti-apoptotic Properties. Neuro Toxicology. 25(1-2):233-242. 2004.
Melis, M. R., Argiolas, A. Dopamine and sexual behavior Original Research Article
Neuroscience & Biobehavioral Reviews, 19(1): 19-38. 1995.

Milgram NW et al., Maintenance on L-deprenyl prolongs life in aged male rats. Life Sciences 47: 415-20, 1990.
Tariot PN et al., L-Deprenyl in Alzheimer’s Disease: Preliminary evidence for behavioral change with monoamine oxidase B inhibition. Archives of General Psychiatry 44: 427-33, 1987.

Weinberger H. Andrea, Erin L. Reutenauer, Peter I. Jatlow, Stephanie S. O’Malley, Marc N. Potenza, Tony P. George. A double-blind, placebo-controlled, randomized clinical trial of oral selegiline hydrochloride for smoking cessation in nicotine-dependent cigarette smokers. Drug and Alcohol Dependence, 107(2-3): 188-195, 2010.
Zeng Yong-Chun, Stefano Bongrani, Elena Bronzetti, Sandro Cadel, Alberto Ricci, Bruno Valsecchi, Francesco Amenta. Influence of long-term treatment with L-deprenyl on the age-dependent changes in rat brain microanatomy Original Research Article
Mechanisms of Ageing and Development, 73(2): 113-126, 1994.


 

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