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Deprenyl-medication: a strategy to modulate the age-related decline of the striatal dopaminergic system 

Knoll J

Department of Pharmacology,
Semmelweis University of Medicine,
Budapest, Hungary. 
J Am Geriatr Soc 1992 Aug; 40(8):839-47

ABSTRACT

Deprenyl (Selegiline, Jumex, Eldepryl, Movergan), a close structural relative to phenylethylamine (PEA), is a drug with a unique pharmacological spectrum. 

(1) It is a highly potent and selective, irreversible inhibitor of B-type monoamine oxidase (MAO), a predominantly glial enzyme in the brain. The activity of this enzyme significantly increases with age. (-)Deprenyl, the first selective inhibitor of MAO-B described in literature, has become the universally used research tool for selectively blocking B-type MAO. It is the only MAO-B inhibitor in clinical use. 

(2) (-)Deprenyl interferes with the uptake of catecholamines and indirectly acting sympathomimetics because it is handled by the catecholaminergic neuron in a way similar to the physiological substances transported through the axonal end organ and vesicular membrane. The unique behavior of (-)deprenyl is that, in striking contrast to PEA and its relatives, it does not displace the transmitter from storage, ie, it is not a releaser.  The net result is that (-)deprenyl inhibits the releasing effect of tyramine, and, at present, is the only safe MAO inhibitor that can be administered without dietary precautions. (

3) Maintenance on (-)deprenyl selectively enhances superoxide dismutase (SOD) and catalase activity in the striatum. This effect is unrelated to its effect on MAO-B and the inhibitory effects of the drug on neurotransmitter uptake. 

(4) Maintenance on (-)deprenyl facilitates the activity of the nigrostriatal dopaminergic neurons with remarkable selectivity, and this effect, too, is unrelated to either its effects on MAO or on neurotransmitter uptake. 

(5) Maintenance on (-)deprenyl prevents the characteristic age-related morphological changes in the neuromelanin granules of the neurocytes in the substantia nigra. All in all, (-)deprenyl increases the activity of the nigrostriatal dopaminergic system and slows its age-related decline. Maintenance of male rats on (-)deprenyl delays the loss of the capacity to ejaculate, slows the decline of learning and memory, and significantly lengthens the life-span as compared with saline-treated rats.  Parkinson's disease patients on levodopa plus (-)deprenyl (10 mg daily) live significantly longer than those on levodopa alone. (-)Deprenyl is the first drug that retards the progress of Parkinson's disease.  Newly diagnosed Parkinson's disease patients maintained on (-)deprenyl need levodopa significantly later than their placebo-treated peers.  Maintenance on (-)deprenyl improves significantly the performance of patients with Alzheimer's disease. It is concluded that Parkinson's disease and Alzheimer's disease patients need to be treated daily with 10 mg (-)deprenyl from diagnosis until death, irrespective of other medication.

Parkinson's research / abstracts

 1.    Deprenyl  effect on cognitive functions in early Parkinson's 
 2.   
Deprenyl  depression in Parkinson's disease
 3.   
Deprenyl  stimulates biosynthesis of cytokines interleukin-1 & 6
 4.    Deprenyl  effect of MAO-B inhibitors on MPP+ toxicity
 5.    Deprenyl  modulates the decline of the dopamineric system
 6.    Deprenyl 
possible mechanisms of action in Parkinson's 
 
7.    Deprenyl  pharmacological basis of the beneficial effects
 8.   
Deprenyl  improves visuo-motor control in early Parkinsonism
 9.   
Deprenyl  delays disability in Parkinsonian patients
10.  
Deprenyl  management of early Parkinson's disease
11.  
Deprenyl  delays the onset of disability in Parkinsonian patients
12.  
Deprenyl  and tocopherol antioxidative therapy of Parkinsonism

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