Platelet Monoamine Oxidase B Activity in “de novo” and L-Dopa Treated Parkinsonian Patients and Controls

Abstract

ABSTRACT:Objective: Previous studies demonstrated controversial results regarding monoamine oxidase B (MAO-B) activity in platelets in the periphery in parkinsonian patients (PD). Subjects and Methods: Therefore we determined platelet MAO-B activity in three age-and sex-matched groups of 17 untreated, so called "de novo" patients with Parkinson's disease (PD), 17 parkinsonian patients, receiving levodopa, and 17 controls by a radio enzymatic assay. Results: No significant differences of MAO-B activity appeared. Conclusion: This result suggests that phenotypic determination of MAO-B activity in platelets may not be used as peripheral marker in PD and that levodopa treatment does not alter MAO-B activity in the periphery. RESUME: Activite de la monoamine oxydase B plaquettaire chez les patients naifs et traites par la L-dopa et chez les controles. Objectif: Les resultats des etudes anterieures concernant l'activite de la monoamine oxydase B (MAO-B) plaquettaire peripherique chez des parkinsoniens (MP) sont controverses. Sujets et methodes: Nous avons done mesure l'activite de la MAO-B plaquettaire par dosage radio-enzymatique chez 3 groupes de 17 patients apparies quant a Page et au sexe, soit 17 parkinsoniens jamais traites par la L-dopa, 17 parkinsoniens recevant de la L-dopa et 17 controles. Resultat: II n'y avait pas de differences significatives dans l'activite de la MAO-B. Conclusion: Ce resultat suggere que la determination de l'activite de la MAO-B plaquettaire ne peut etre utilised comme marqueur du patient dans la MP et que le traitement par la L-dopa ne modifie pas l'activite peripherique de la MAO-B.Can. J. Neurol. Sci. 1998; 25: 249-251 Various enzymes, such as catechol-O-methyl transferase or monoamine oxidase (MAO) metabolise biogenic amines, e.g., dopamine, in the brain. MAO can be differentiated biochemically and pharmacologically into two forms (types A and B) with different substrate specificities and inhibitor sensitivities. Animal studies have indicated that MAO-A is mainly, but not exclusively, located in brain neurons, such as neurons of the locus coerulus, while MAO-B is preferentially found in serotonergic neurons, glia and astrocytes.12 Elevated levels of MAO-B were found in the substantia nigra of parkinsonian patients. Estimation of peripheral blood cell activities of monoamine oxidase B may reflect central enzyme activity. Therefore platelets were often used as source for MAO-B estimation in the periphery in in vivo studies.34 MAO-B is potentially relevant to an oxidative stress model of Parkinson's disease (PD) causation, because catabolism of catecholamines via monoamine oxidase B (MAO-B) may generate hydrogen peroxide.5 Hydrogen peroxide is converted to highly reactive hydroxyl radicals after reaction with transition metals. 6 Free radical formation and disturbed detoxification processes may be essential contributors to the pathogenesis of Parkinson's Disease (PD).The aim of this study was to investigate, whether chronic levodopa application may induce changes of MAO-B activity, ...

Comparative platelet proteome analysis reveals an increase of monoamine oxidase-B protein expression in Alzheimer's disease but not in non-demented Parkinson's disease patients

“…However, there are even more conflicting results concerning changes in platelet Mao-B activity in patients with PD as compared to the situation in ageing in general and AD patients in particular. The body of evidence regarding Mao-B activity being altered in PD patients is controversial [9,[56][57][58][59][60][61], albeit a study that quantified the amount of Mao-B in platelets of PD patients by ELISA did not find any changes in protein expression [62]. Likewise, our collective of idiopathic non-demented PD patients did not show any Mao-B expression change compared to sex-and age-matched healthy controls, as observed by applying in 2D DIGE and 1D Western blot.…”

“…However this is not very likely since previous studies demonstrated that naïve PD patients and PD patients receiving levodopa did not differ significantly in their platelet Mao-B activity [57,58]. Interestingly, the two PD patients also receiving additional the aforementioned Mao-B inhibitor selegiline [63] similarly did not show noticeable changes in the Mao-B expression.…”

Altered Platelet Monoamine Oxidase-B Activity in Idiopathic Parkinson’s Disease

“…Variation in the activity has been attributed due to different substrate and relative activity defect in platelet MAO-B from Parkinson's disease patients [36]. However, Kuhn et al [37] found no significant change in the activity of platelet MAO-B both in de novo and L-DOPA treated Parkinson's patients. As there are several reports on the polymorphism of this enzyme [30,[38][39][40][41][42], the present study was undertaken to investigate the platelet MAO-B activity in Indian cases of Parkinson's disease.…”