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(-)Deprenyl in perspective: prophylaxis for Parkinson's disease?
Journal of Neural Transmission. Supplementum
|January 1, 1986
Summary
Environmental toxins like MPTP may cause Parkinson's disease. Early detection using enzyme activity markers and PET scans could enable treatment with MAO B inhibitors, potentially slowing disease progression.
Area of Science:
- Neuroscience
- Environmental Toxicology
- Pharmacology
Background:
- Idiopathic Parkinson's disease (PD) may be linked to environmental neurotoxins, such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).
- Monoamine oxidase B (MAO B) metabolizes MPTP into the potent neurotoxin 1-methyl-4-phenylpyridinium (MPP+).
- MAO B inhibitors, like (-)deprenyl, can block this conversion and show preliminary efficacy in PD treatment.
Purpose of the Study:
- To identify biomarkers for detecting premorbid Parkinson's disease.
- To explore strategies for early intervention with MAO B inhibitors prior to disease manifestation.
- To investigate methods for identifying individuals who might benefit from long-term (-)deprenyl treatment.
Main Methods:
- Monitoring enzymatic activity of phenolsulphotransferase and MAO B as potential markers.
- Utilizing Positron Emission Tomography (PET) scans with 6-18F-labelled dopa.
- Assessing the neurotoxic conversion of MPTP by MAO B and its inhibition by (-)deprenyl.
Main Results:
- Preliminary evidence suggests (-)deprenyl can interrupt the pathological process in Parkinson's disease.
- MAO B plays a crucial role in converting MPTP to its toxic form, MPP+.
- Overactivity of dopamine-degrading enzymes may serve as a premorbid marker.
Conclusions:
- Identifying individuals in the premorbid stage of Parkinson's disease is critical for effective early intervention.
- Monitoring MAO B and phenolsulphotransferase activity, alongside PET imaging, offers promising avenues for early PD detection.
- Early treatment with MAO B inhibitors like (-)deprenyl may halt disease progression and improve life expectancy.