Biomedical subjects

H Przuntek

Publications and source records attributed to H Przuntek.

At least 55 records · Page 3Linked to original sources

PubMed2001

Familial parkinsonism with synuclein pathology: clinical and PET studies of A30P mutation carriers.

BACKGROUND: The authors identified the second known mutation in the alpha-synuclein(SNCA) gene, an alanine-to-proline exchange in amino acid position 30 (A30P), that cosegregates with the disease in one German family with autosomal dominantly inherited parkinsonism (ADP). The authors studied carriers of the A30P mutation to compare the phenotype of this mutation with idiopathic PD (IPD) and to assess nigrostriatal dopaminergic function in symptomatic and preclinical mutation carriers. METHODS: The pedigree of the A30P family spans five generations with five affected individuals. The authors performed detailed neurologic examinations followed by mutation analysis in 11 living individuals. In three mutation carriers, two individuals with definite PD and one person at risk for PD, they used L-[18]F-fluoro-3,4-dihydroxyphenylalanine (F-DOPA), [11]C-raclopride (RAC), and [18]F-fluorodeoxyglucose (FDG) PET to investigate presynaptic dopaminergic function, dopamine D2 receptors, and cerebral energy metabolism. The authors studied the cognitive functions of carriers of the A30P mutation using neuropsychological screening. RESULTS: PET studies revealed striatal presynaptic dopaminergic alterations consistent with sporadic IPD in two affected family members and no evidence for nigrostriatal dopaminergic dysfunction in one presymptomatic mutation carrier. Neuropsychological testing in four mutation carriers provided evidence for cognitive impairment as a frequent and early symptom of the A30P mutation; this is also supported by regional cerebral energy metabolism alterations in the clinically presymptomatic subject. CONCLUSIONS: The phenotype of the A30P mutation in the SNCA gene is similar to that of sporadic IPD, including a high variability of the age at disease onset, ranging from 54 to 76 years. The follow-up of presymptomatic carriers of the A30P mutation may give insight into preclinical disease stages and early manifestations of PD.

Aged↗

PubMed2001

Integrity of the blood-cerebrospinal fluid barrier in early Parkinson's disease.

Dysfunction of the blood-cerebrospinal fluid barrier (BCB) has been implicated in the pathogenesis of Parkinson's disease (PD) and other neurodegenerative disorders. Therefore, we assayed serum and cerebrospinal fluid (CSF) from 30 parkinsonian patients and 30 controls for concentrations of albumin and IgG. The CSF/serum ratio for albumin (AQ), IgG (GQ), IgG-index as well as determination of oligoclonal bands were used to evaluate BCB function and to quantify humoral immune response within the central nervous system (CNS). Levels of AQ, GQ and IgG-index did not significantly differ in both groups. We found no dysfunction of the blood-CSF barrier or signs of local synthesis of IgG in the central nervous system of parkinsonian patients. Our data do not support the hypothesis of a dysfunctional BCB that contributes to pathophysiological mechanisms underlying PD.

Adult↗

PubMed2001

Double-blind crossover trial of trimethoprim-sulfamethoxazole in spinocerebellar ataxia type 3/Machado-Joseph disease.

OBJECTIVE: To evaluate the efficiency of a combination of trimethoprim and sulfamethoxazole in patients with spinocerebellar ataxia type 3/Machado-Joseph disease (SCA3/MJD). DESIGN: Placebo-controlled, double-blind crossover trial in 22 patients with genetically confirmed SCA3/MJD. Study phases of 6 months were separated by a washout period of 4 weeks. Dosages were a combination of trimethoprim, 160 mg, and sulfamethoxazole, 800 mg, twice daily for 2 weeks, followed by a combination of trimethoprim, 80 mg, and sulfamethoxazole, 400 mg, twice daily for 5.5 months. SETTING: Outpatient department of the Neurological Clinic, Ruhr-University, Bochum, Germany. MAIN OUTCOME MEASURES: Ataxia ranking scale, self-assessment score, static posturography, and results of motor performance testing. Effects on the visual system were studied using the achromatic Vision Contrast Test System and the Farnsworth-Munsell 100-hue test for color discrimination. Physical and mental health were documented using the Medical Outcomes Study 36-Item Short-Form Health Survey. Subgroup analyses assessed the influence of age, sex, age at onset, duration of the disease, phenotype, and CAG repeat length on test performance. RESULTS: Twenty of 22 patients completed the study. Dropouts were due to a rash (placebo phase) and an attempted suicide in a family conflict. Trimethoprim-sulfamethoxazole therapy had no significant effect in SCA3/MJD patients in the short-term analysis (2 weeks) or in the long-term interval (6 months). CONCLUSIONS: In contrast to previous reports that studied smaller groups of patients, treatment with trimethoprim-sulfamethoxazole did not improve the diverse and complex movement disorders caused by SCA3/MJD. Trimethoprim-sulfamethoxazole had no effect on the visual system and cannot be recommended as a continuous treatment for SCA3/MJD patients.

Adult↗

PubMed2001

Multiple sclerosis: modulation of apoptosis susceptibility by glatiramer acetate.

OBJECTIVES: We investigated whether therapy of multiple sclerosis (MS) with glatiramer acetate (GA) involves the modulation of programmed cell death (apoptosis) in disease-relevant T-helper lymphocytes. MATERIAL AND METHODS: Blood was drawn from 15 relapsing-remitting MS patients both before (baseline) as well as 6, 12, and 18 weeks after GA therapy and from 15 healthy controls. Detection of apoptosis was performed in response to in vitro stimulation with GA, myelin basic protein or medium alone. RESULTS: T-helper lymphocytes from untreated MS patients displayed an overall increased apoptosis susceptibility in vitro, compared to controls. During subsequent GA therapy, apoptosis vulnerability of these T cells in MS patients significantly declined under the initial baseline before treatment, and was finally equal in treated patients and controls. GA itself had no direct apoptosis-modulatory properties in vitro. CONCLUSION: Our findings indicate that therapy of multiple sclerosis with glatiramer acetate presumably involves the compensation of altered apoptosis in T-helper lymphocytes.

Adult↗

PubMed2001

Vascular Parkinsonism: a case report and review of the literature.

Vascular Parkinsonism (VP) is characterised by sudden onset and rapid progression of clinical symptoms, absent or poor response to dopamine substitution therapy, and postural instability with shuffling gait and absence of tremor, making it a clinically distinct entity from idiopathic Parkinson's disease (IPD). Furthermore, it displays certain typical findings in neurological investigations. We report on a patient presenting features of VP associated with an intracerebral lesion not ascribed to VP to date, namely an isolated ischaemic focal lesion located in the left cerebral peduncle between the substantia nigra and nucleus ruber as evidenced by magnetic resonance imaging (MRI). The pathophysiological organic correlate for contralateral extrapyramidal symptoms in this patient may be an interruption of nigro-thalamic projection, interrupting the final subcortical station in the cortic-striato-pallido-nigro-thalamico-cortical loop central to the pathophysiology of parkinsonian syndromes. Non-response t o levodopa therapy could be a consequence of disruption of the cortico-basal ganglia-cortical loop on account of ischaemic destruction of subcortico-cortical axons, the underlying pathology, therefore, not being the result of a loss of nigral dopaminergic neurons or striatal dopamine deficiency pathogonomonic of IPD. To our knowledge, this is the first case of clinically manifest VP to be described with a single lesion in the contralateral cerebral peduncle between the substantia nigra and nucleus ruber, and suggests alternative intracerebral patterns for the distribution of disease-causing lesions in VP, and possibly new pathophysiological explanations for the nature of this disease.

Basal Ganglia Diseases↗

PubMed2001

SPECT imaging with [123I]-beta-CIT in Parkinsonism: comparison of SPECT images obtained by a single-headed and a three-headed gamma camera.

Single photon emission computed tomography (SPECT) imaging of dopamine transporters by using the cocaine derivative [123I]-(1R)-2-beta-carbomethoxy-3-beta-(4-iodophenyl)-tropane ([123I]-beta-CIT) has been shown to be useful in patients with Parkinsonism. The aim of this study was to compare beta-CIT imaging with single-headed (SHS) and three-headed gamma camera systems (THS). In 17 patients with Parkinsonism, SPECT imaging with an SHS and a THS was performed 24 h after injection of 180 MBq of [123I]-beta-CIT. The SPECT studies were evaluated by visual assessment of the caudate nucleus (CN) and the putamen (PT) and the calculation of the striatal/cerebellar (S/C) ratios (with additional comparison to clinical symptoms measured by the Unified Parkinson's Disease Rating Scale (UPDRS)). The S/C ratios measured by the SHS and THS showed highly significant correlation (two-tailed P < 0.01) with Spearman correlation coefficients (SCCs) of 0.864 for the right side, 0.676 for the left side, and 0.761 for both sides. By the SHS, a sufficient visual differentiation between the CN and the PT could not be achieved. A significantly better distinction could be achieved by using the THS (Wilcoxon P<0.05). The S/C ratios of the THS only showed a significant (P < 0.05) SCC of -0.514 comparing to the UPDRS. Pathological alterations in the beta-CIT uptake pattern could be identified by using the SHS, but a significantly better differentiation of CN and the PT was possible by using the THS. The significant correlation of the S/C ratios measured by THS only emphasizes the value of THS in beta-CIT imaging.

Aged↗

PubMed2001

Ultrasonic assessment of physiological echo-contrast agent distribution in brain parenchyma with transient response second harmonic imaging.

OBJECTIVES: The present study was designed to provide normal data of transient response second harmonic imaging (TRSHI) examinations of cerebral echo contrast enhancement using different modes of electrocardiogram (ECG) gating and echo-contrast agent doses. MATERIALS AND METHODS: Fifty-five patients were examined in an axial diencephalic plane of section using the transtemporal acoustic bone window. TRSHI examinations (ECG gating: systolic, frame-rate once every 2 cardiac cycles = "basical instrument setting") could be performed in 50 individuals with adequate insonation conditions after application of 4 g of a galactose-based microbubbles suspension in a concentration of 400 mg/ml. For comparison, diastolic ECG gating (20 patients), cardiac-cycle triggering frequency of once every 2 seconds (15 patients), or an echo contrast agent dose of 2 g Levovist (15 patients) were used. Analysis of peak intensities (PIs) and areas under the curve (AUCs) was done in posterior (region of interest [ROI]a) and anterior (ROIb) parts of the thalamus, in the lentiform nucleus (ROIc), and the white matter (ROId). RESULTS: In 41 patients with basical instrument setting, characteristic time intensity curve (TIC) could be detected in all ROIs. In ROIa (90%) and ROIb (82%), focal contrast enhancement was most difficult to visualize, and in ROIc and ROId, characteristic TICs were observable in more than 90% of the examinations. Background subtracted PIs and AUCs were significantly higher in ROIc (mean PI: 12.2 +/- 8 acoustic units [AUs]; mean AUC: 598.8 +/- 451.1 AU x Cardiac cycles), and ROId (11.8 +/- 6.9; 559.2 +/- 404) as compared to ROIa (8.3 +/- 5.2; 368.9 +/- 242.7) and ROIb (7.1 +/- 4.7; 298.2 +/- 199.1) (P < .0001). Values for corresponding examinations with a diastolic ECG gating and a cardiac cycle triggering frequency of once every 2 seconds were not different as compared to the basical instrument setting. A 4 g Levovist dose increased the portion of typical TIC in all ROIs. PI of 4 g examinations were significantly higher in ROId and ROIb as compared to the 2 g examination. CONCLUSION: Our findings indicate that TRSHI allows noninvasive assessment of focal cerebral contrast enhancement in the majority of patients with adequate insonation conditions. This study provides data about normal quantitative and qualitative TRSHI values in patients without cerebrovascular diseases. A dose of 4 g Levovist is recommended in those individuals with inaccurate echo contrast enhancement using the 2 g dose.

Adult↗

PubMed2001

Relation between electroconvulsive therapy, cognitive side effects, neuron specific enolase, and protein S-100.

OBJECTIVE: To investigate whether electroconvulsive therapy (ECT) induces brain tissue damage expressed as an increase in neuron specific enolase and protein S-100. METHODS: A total of 179 serial measurements of S-100 and NSE serum concentrations were performed on 14 patients during the course of a bilaterally stimulated ECT series. Cognitive performance was assessed by psychometric testing carried out on the day before the start of ECT as well as on the days after the third, sixth, and last ECT. Pre-ECT and post-ECT concentrations of NSE and S-100 were compared by non-parametric tests. RESULTS: On average, 9.5 (SD 2.9) (range 3-12) ECTs were applied; 13 of 14 patients received at least six ECTs. The average duration of convulsion (computed for all ECTs) was 29.0 (SD 10.5) seconds. At no point during the ECT series was there a significant increase in the average NSE or S-100 concentrations compared with the baseline investigation before the start of the ECT series. The maximal measured post-ECT values of NSE and S-100 were 26.6 ng/ml and 0.46 ng/ml, respectively. The cumulative energy doses applied, seizure durations, and ECT induced changes in cognitive performance scores were never significantly correlated with the NSE or S-100 serum concentrations. CONCLUSION: This pattern of findings suggests that a modern ECT, fulfilling current quality standards, induces no brain tissue damage detectable by changes in NSE or protein S-100.

Adult↗

PubMed2000

Choice reaction time after levodopa challenge in parkinsonian patients.

Various types of choice reaction time paradigms demonstrated deficits in the preparation and execution of movements in parkinsonian subjects. These studies showed controversial results, since they included parkinsonian individuals being: (i) previously untreated; (ii) off; or (iii) on anti-parkinsonian medication. Moreover, these trials do not take into consideration the acute effects of levodopa administration. Objective of this study was to determine the effect of long-term dopaminergic substitution therapy within a standardized levodopa challenge test in combination with a repeatedly performed choice reaction time task in parkinsonian individuals. Parkinsonian participants consisted of previously untreated, so-called "de-novo" patients and of individuals, who were chronically substituted with dopaminergic drugs, but were taken off medication for at least 12 h. All participants took 250 mg levodopa/benserazide after assessment of baseline data. Then we repeatedly measured choice reaction- and movement time within the next 90 min. No significant change of the assessed task data appeared in the "de-novo" group, but reaction- and movement time significantly shortened in previously treated subjects. Sedative effects of levodopa and/or dopaminergic overstimulation hypothetically explain the results of the previously untreated patients, whereas long-term dopaminergic substitution therapy hypothetically causes tolerance to these phenomena in treated parkinsonian individuals. Future studies on parkinsonian subjects should discuss their results on the basic pathophysiology or basal ganglia dysfunction in the light of a putative impact of long-term anti-parkinsonian drug therapy.

Adult↗

PubMed2000

Genetic analysis of the alpha2-macroglobulin gene in early- and late-onset Parkinson's disease.

Recent association studies investigating polymorphisms in the alpha2-macroglobulin (A2M) gene provided evidence for an involvement of this protease inhibitor in the pathogenesis of Alzheimer's disease (AD). The partially overlapping pathology between AD and Parkinson's disease (PD) led us to investigate the role of A2M in PD. We performed association studies in a large sample of 328 German PD patients and 322 closely matched healthy controls. Analyzing the Val1000Ile polymorphism and a pentanucleotide deletion in the 5' splice site of exon 18 of the A2M gene we found an excess of homozygosity for the A2M deletion in early-onset PD (EOPD) patients (age at onset < 50 years) compared to late-onset PD (LOPD) patients (age at onset > 50 years; p = 0.008, p(p)c = 0.064, chi2 = 7.017). Therefore our data might indicate an age at onset modulating effect of the homozygous A2M deletion in PD.

Age of Onset↗

PubMed2000

Mutation analysis and association studies of the UCHL1 gene in German Parkinson's disease patients.

Recently, an Ile93Met substitution has been identified in the ubiquitin carboxy-terminal hydrolase L1 (UCHL1) gene in a single German PD family with autosomal dominant inheritance. To determine whether mutations in the UCHL1 gene are causative for Parkinson's disease (PD) a detailed mutation analysis was performed in a large sample of German sporadic and familial PD patients. We found no disease-causing mutation in the coding region of the UCHL1 gene. Direct sequencing revealed six intronic polymorphisms in the UCHL1 gene. Analysis of an S18Y polymorphism in exon 3 of the UCHL1 gene in sporadic PD patients and controls showed carriers of allele 2 (tyrosine) significantly less frequent in patients with a reduced risk of 0.57 (CI = 0.36-0.88; p = 0.012, p(c) = 0.047, chi2 = 6.31). Our study shows that sequence variations in the coding region of UCHL1 are a rare event. A protective effect of a certain UCHL1 variant in the pathogenesis of sporadic PD is suggested, underlining the relevance of UCHL1 in neurodegeneration.

Aged↗

PubMed2000

Extrapyramidal motor signs in degenerative ataxias.

BACKGROUND: Extrapyramidal motor signs (EPS) are well-known symptoms of degenerative ataxia. However, little is known about frequency and appearance of EPS in subtypes of ataxia. METHODS: We characterized 311 patients with ataxia clinically and genetically. Course of the disease and EPS were investigated according to a standardized protocol. Diagnostic and prognostic impact of EPS in subtypes of ataxia was analyzed by Kaplan-Meier plots. RESULTS: Extrapyramidal motor signs occurred in all forms of ataxia, but frequency and type of EPS varied between genetically and clinically defined subtypes. Postural tremor in hereditary ataxias was typical for spinocerebellar ataxia type 2 (SCA2). Dystonia was generally rare in ataxias, but, if present, suggested SCA3. We observed a parkinsonian variant of SCA3 in which parkinsonism was present in the beginning of the disease and responded well to levodopa therapy, leading to diagnostic confusion. Parkinsonism in SCA3 was independent of CAG repeat length but ran in families, suggesting modifying genes. In idiopathic sporadic cerebellar ataxia (ISCA), EPS are more frequent in late-onset than in early-onset forms. In 50% of ISCA patients with parkinsonism, the diagnosis of multiple system atrophy remained questionable because of normal autonomic function. CONCLUSIONS: Extrapyramidal motor signs can help to predict the genetic subtype of ataxia. Extrapyramidal motor signs were more frequent in genetic subtypes in which basal ganglia affection has been demonstrated by postmortem studies. However, no type of EPS was specific for an underlying mutation. In ISCA, EPS are an adverse prognostic factor. Parkinsonism is especially associated with a more rapid course of the disease. Arch Neurol. 2000;57:1495-1500

Aged↗

PubMed2000

Non-dopaminergic therapy in Parkinson's disease.

Parkinson's disease no longer seems to be a disease entity caused by only one pathogenetic factor. The facile characterization of Parkinson's disease as a more or less isolated disorder of the dopaminergic system proves to be an unacceptable oversimplification of the pathology of the disease. Characteristically, not all dopaminergic systems of the central nervous system are involved in the degenerative process. In addition to the nigrostriatal dopaminergic pathway, parts of the glutamatergic, cholinergic, tryptaminergic, noradrenergic, adrenergic, serotonergic, and peptidergic neurons show serious cytoskeletal damage. In the light of these findings, drugs influencing these transmitter systems should be useful in the treatment of parkinsonian symptoms. For this reason, non-dopaminergic drugs are gaining more and more importance. Besides the theoretically interesting adenosine A2 receptor antagonists, budipine, a polyvalent potent new antiparkinsonian drug, has been tested in clinical studies. Budipine is a potent non-dopaminergic antiparkinsonian drug with pharmacological effects that are not comparable to those of conventional drugs applied in Parkinsonian pharmacotherapy. Budipine experimentally increased the brain content of noradrenaline, dopamine, serotonin, and histamine. The dopamine, serotonin, noradrenaline, gamma aminobutyric acid (GABA), and endorphine receptor affinities were not altered, but N-methyl-D-aspartate (NMDA) and sigma receptor affinities were increased as shown by in vivo and in vitro trials with budipine. MPTP (N-methyl-4-phenyl- 1,2,3,6-tetrahydropyridine) and MPP+ antagonistic effects have also been demonstrated. Budipine also shows neuroprotective as well as symptomatic antiparkinsonian effects. In two randomized, double-blind, multicenter, placebo-controlled studies, relevant therapeutic effects have been observed in previously untreated, so-called "de-novo" parkinsonian patients and in subjects in later stages of the disease. Budipine significantly reduces akinesia, rigidity, and tremor. Optimal effects of budipine can be seen 4-6 weeks after starting treatment with this substance. Budipine can be added to all available antiparkinsonian drugs. An open, prospective, long-term study of 2532 patients with Parkinson's disease (Study BY701/01A) confirmed the favorable safety and tolerability profiles of budipine.

Dopamine↗

PubMed2000

Genetic background of apparently idiopathic sporadic cerebellar ataxia.

Disease-causing mutations have been identified in various entities of autosomal dominant ataxia and in Friedreich's ataxia. However, no molecular pathogenic factor is known to cause idiopathic cerebellar ataxias. We investigated the CAG/CTG trinucleotide repeats causing spinocerebellar ataxia types 1, 2, 3, 6, 7, 8 and 12, and the GAA repeat of the frataxin gene in 124 patients apparently suffering from idiopathic sporadic ataxia, including 20 patients with the clinical diagnosis of multiple system atrophy. Patients with a positive family history, a typical Friedreich phenotype, or symptomatic ataxia were excluded. Genetic analyses uncovered the most common Friedreich mutation in 10 patients with an age at onset between 13 and 36 years. The SCA6 mutation was present in nine patients with disease onset between 47 and 68 years of age. The CTG repeat associated with SCA8 was expanded in three patients. One patient had SCA2 attributable to a de novo mutation from a paternally transmitted, intermediate allele. We did not identify the SCA1, SCA3, SCA7 or SCA12 mutation in idiopathic sporadic ataxia patients. No trinucleotide repeat expansion was detected in the MSA subgroup. This study has revealed the genetic basis in 19% of apparently idiopathic ataxia patients. SCA6 is the most frequent mutation in late onset cerebellar ataxia. The frataxin trinucleotide expansion should be investigated in all sporadic ataxia patients with onset before age 40, even when the phenotype is atypical for Friedreich's ataxia.

Age of Onset↗

PubMed2000

Motor performance: normative data, age dependence and handedness.

Quantitative, apparatus-based assessment of motor performance is a useful tool when addressing questions of therapy evaluation, quality control and early detection of movement disorders. Until now, few such methods have been sufficiently standardised to allow their routine employment in the clinic. Before assessing the impaired performance of patients, the first stage of standardisation is the determination of criteria of normal performance in healthy subjects. We have standardised a multidimensional test battery for motor performance of the upper extremities (Schoppe's "motorische Leistungs-Serie" = MLS). On the basis of the performance of 80 healthy controls, normative algorithms which allow correction of performance with reference to age were calculated. Further, our investigation provided information concerning the complexity of normal motor performance and the question of laterality (handedness). Standardised apparatus-based quantification of performance promises to be a valuable supplement to rating scales in the evaluation of patient motor skills, particularly in the early stages of their illness.

Adult↗

PubMed2000

The activity of catechol-O-methyltransferase in parkinsonian patients with "on-off fluctuations".

Motor fluctuations complicate therapy in Parkinson's disease (PD). The mechanisms responsible for motor fluctuations such as the on-off type, are poorly understood. Differences of activity of various enzymes, such as Catechol-O-Methyltransferase (COMT, E.C.2.1.1.6.) may influence the appearance of motor fluctuations and the quantity of metabolic products of levodopa. Aim of this study was to compare erythrocyte COMT-activity in Parkinsonian patients without and with motor fluctuations from the on-off type. No significant differences in COMT-activity appeared in both groups. We conclude that activity differences in COMT-activity do not contribute to the appearance of motor fluctuations in Parkinson's disease.

Aged↗

PubMed2000

Tolcapone increases maximum concentration of levodopa.

No significant increase of the maximum concentration (Cmax) of levodopa after addition of catechol-O-methyltransferase inhibitor tolcapone occurred in previous pharmacokinetic studies predominantly on healthy volunteers. We compared pharmacokinetics of levodopa in plasma before and after addition of tolcapone in 13 treated parkinsonian subjects under standardized conditions. We found a significant increase of Cmax of levodopa after the addition of tolcapone. This may represent one cause for the occurrence of dyskinesia previously early in the course of treatment with tolcapone.

Aged↗

PubMed2000

Glutathione S-transferase polymorphism in Parkinson's disease.

Glutathione S-transferases (GSTs) are involved in the detoxification of endogenous or exogenous toxins, which may play a role in the pathogenesis of Parkinson's disease. We genotyped the Glutathione-S-Transferase isoenzymes GSTM1 and GSTT1 by polymerase chain reaction in order to evaluate different gene polymorphisms of these isoenzymes in 149 parkinsonian and 99 control subjects. No differences appeared between both groups regarding the frequencies of the homozygous deletion of GSTM1 (odds ratio 1.021; 95% CI [0.613; 1.699], p < 0.521 Fisher's exact test) and GSTT1 (odds ratio 1.514; 95% CI [0.811; 2.824], p < 0.127). Age of onset of PD did not correlate to GSTM1 and GSTT1 polymorphisms. These results do not support the hypothesis of a possible impact of GSTM1 and GSTT1 detoxification activities in the pathogenesis of Parkinson's disease.

Adult↗