2005 issue 2

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Volume 14, issue 2

Review article

The ways of neuroprotection in Parkinson 's disease as exemplified by rasagiline

Danuta Turzyńska1, ANNA SKÓRZEWSKA1, Alicja Sobolewska1, Adam Płaźnik1,2
1. Zakład Neurochemii Instytutu Psychiatrii i Neurologii w Warszawie
2. Katedra i Zakład Farmakologii Doświadczalnej i Klinicznej w Warszawie
Postępy Psychiatrii i Neurologii 2005; 14 (2): 131-136
Keywords: Parkinson's disease, neurodegeneration, neuroprotection, rasagiline

Abstract

Objective. The aims of the paper were: to present neurodegenerative factors involved in the pathomechanism of Parkinson 's disease, to outline the role of neuroprotection, and to evaluate antiapoptotic properties of rasagiline on the grounds of pre-clinical trials.

Review. Parkinson 's disease is one of the most widespread neurodegenerative disorders. An apoptotic mechanism of cell death is considered to predominate in Parkinson 's disease. In the process of apoptosis the mitochondrial membrane potential reduction is followed by opening of the mitochondrial permeability transition pore. These processes result in disturbance of mitochondrial Ca2+ homeostasis, release of cytochrome C, and activation of caspase 3, finally leading to cell death by apoptosis. At present new drugs are sought that would inhibit neurodegenerative processes at the molecular cell level. Rasagiline is a selective, irreversible, second-generation inhibitor of monoamine oxidase type B (MAO-B). Numerous pre-clinical trials suggest that this drug not only inhibits MAO-B enzyme, but also has neuroprotective and antiapoptotic properties. Regulating the mitochondrial membrane potential rasagiline affects the functions and expression of mitochondrial proteins, which eventually prevents neurodegeneration.

Conclusions. Both pre-clinical and preliminary clinical trials suggest that rasagiline is effective not only in the treatment ofParkinson 's disease symptoms, but also affects the pathomechanism underlying the developing condition.

Address for correspondence:
Prof. Adam Płaźnik, Zakład Neurochemii Instytutu Psychiatrii i Neurologii, ul. Sobieskiego 9, 02-957 Warszawa, e-mail: adaplaz@yahoo.com