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Biomedical subjects

M A Kuiper

Publications and source records attributed to M A Kuiper.

30 records · Page 2Linked to original sources
PubMed1994

Phenytoin parahydroxylation is not impaired in patients with young-onset Parkinson's disease.

Impaired hepatic detoxification capacity by cytochrome P450 subsystems has been implicated in the pathogenesis of Parkinson's disease. We have demonstrated that hepatic parahydroxylation of phenytoin (PHT) is impaired in patients with late-onset Parkinson's disease. In the present study, we have investigated the hypothesis that PHT parahydroxylation is even more impaired in patients with young-onset Parkinson's disease (age at onset before 40 years). We determined PHT parahydroxylation capacity in 21 patients with young-onset Parkinson's disease and 15 healthy age-matched controls. PHT parahydroxylation capacity was assessed by measuring the ratio of PHT to its major metabolite p-hydroxyphenyl-phenylhydantoin in serum 6 h after an oral test dose of 300 mg PHT. PHT parahydroxylation did not differ significantly between patients and controls. These results argue against the hypothesis that impaired activity of the cytochrome P450 isoenzyme responsible for PHT parahydroxylation is involved in the etiology of Parkinson's disease.

Administration, Oral↗
PubMed1993

Seymour stick.

Explore the source record for details and available documents.

Canes↗
PubMed1993

Multiple system atrophy and progressive supranuclear palsy. Diminished striatal D2 dopamine receptor activity demonstrated by 123I-IBZM single photon emission computed tomography.

OBJECTIVE: To measure D2 dopamine receptors in the striatum in patients with multiple system atrophy and progressive supranuclear palsy by I 3-iodo-6-methoxybenzamide labeled with iodine I 123 (123I-IBZM) single photon emission computed tomography and differentiate them from control subjects. DESIGN: Survey with the following as retrospective criterion standards: (1) parkinsonism, (2) negative apomorphine test, and (3) no or only slight reaction to dopaminergic medication. SETTING: Ambulatory or hospitalized care in an academic referral center. PATIENTS AND CONTROL SUBJECTS: Twenty-one patients with parkinsonism not responding to dopaminergic medication (17 with multiple system atrophy and four with progressive supranuclear palsy) and 21 control subjects without parkinsonism. INTERVENTION: In vivo imaging by single photon emission computed tomography using the D2 dopamine receptor specific radioligand 123I-IBZM. MAIN OUTCOME MEASURE: Striatum/occipital cortex ratio of count rate density as semiquantitative measurement for striatal D2 dopamine receptor density. RESULTS: A highly significant loss of striatal uptake of 123I-IBZM was observed in the patients in comparison to the control subjects with little or no overlap between values. CONCLUSIONS: The hypothesized loss of D2 receptors in multiple system atrophy has been confirmed. Use of 123I-IBZM single photon emission computed tomography may be a cost-effective alternative to positron emission tomography in the differential diagnosis of parkinsonism and in the selection of patients for dopaminergic therapy.

Adult↗
PubMed1993

Serum alpha 1-antichymotrypsin is not a useful marker for Alzheimer's disease or dementia in Parkinson's disease.

We measured serum alpha 1-antichymotrypsin (ACT) levels in patients with Alzheimer's disease (AD), Parkinson's disease (PD), Multiple System Atrophy (MSA) and age-matched controls to evaluate whether serum ACT levels in AD patients were elevated and whether ACT levels in PD patients with dementia differed from those in PD or AD. None of the patient groups displayed an increase in ACT levels. We conclude that serum ACT is not useful as a marker, nor in AD nor in dementia in PD.

Aged↗
PubMed1993

Whole blood monoamine oxidase activity in Parkinson's disease and multiple system atrophy patients.

Monoamine oxidase type B (MAO-B), which catalyses the breakdown of dopamine (DA) in human brain, is said to be involved in the pathophysiology of Parkinson's disease (PD). Activity of MAO-B in PD has been measured in platelets isolated from blood samples in different studies, with contradictory results, possibly due to the differences in substrate used or to differences in platelet isolation. Therefore we measured MAO activity in whole blood, which is almost identical to MAO-B activity in platelets, in 25 drug-naive PD patients, 25 treated PD patients, 9 multiple system atrophy (MSA) patients and 20 controls, using a spectrofluorimetric method with kynuramin as a substrate. No statistically significant differences between groups were found, nor any correlation with the severity or duration of the disease.

Aged↗
PubMed1993

Re-evaluation of cerebrospinal fluid angiotensin-converting enzyme activity in patients with 'probable' Alzheimer's disease.

Angiotensin-converting enzyme activity was measured in lumbar cerebrospinal fluid from patients with 'probable' Alzheimer's disease (n = 17) and age-matched controls (n = 19), using a spectrofluorimetric method. In contrast to a previous finding, no statistically significant difference in the mean (specific) angiotensin-converting enzyme activity was found between the two groups. No correlation existed between (specific) enzyme activity and severity of dementia in the Alzheimer's disease patients. We conclude that angiotensin-converting enzyme in cerebrospinal fluid does not appear to be useful as a potential antemortem marker for Alzheimer's disease.

Aged↗
PubMed1993

X-linked borderline mental retardation with prominent behavioral disturbance: phenotype, genetic localization, and evidence for disturbed monoamine metabolism.

We have identified a large Dutch kindred with a new form of X-linked nondysmorphic mild mental retardation. All affected males in this family show very characteristic abnormal behavior, in particular aggressive and sometimes violent behavior. Other types of impulsive behavior include arson, attempted rape, and exhibitionism. Attempted suicide has been reported in a single case. The locus for this disorder could be assigned to the Xp11-21 interval between DXS7 and DXS77 by linkage analysis using markers spanning the X chromosome. A maximal multipoint lod score of 3.69 was obtained at the monoamine oxidase type A (MAOA) locus in Xp11.23-11.4. Results of 24-h urine analysis in three affected males indicated a marked disturbance of monoamine metabolism. These data are compatible with a primary defect in the structural gene for MAOA and/or monoamine oxidase type B (MAOB). Normal platelet MAOB activity suggests that the unusual behavior pattern in this family may be caused by isolated MAOA deficiency.

Adult↗
PubMed1992

Decreased levels of soluble amyloid beta-protein precursor in cerebrospinal fluid of live Alzheimer disease patients.

The amyloid beta-protein is deposited in senile plaques and the cerebrovasculature in Alzheimer disease (AD). Since it is derived from proteolytic processing of its parent protein, the amyloid beta-protein precursor (APP), we investigated whether levels of the secreted forms of APP are altered in cerebrospinal fluid (CSF) of AD patients. Quantitative immunoblotting studies with the anti-APP monoclonal antibody P2-1 revealed that probable AD patients had markedly lower CSF APP levels than did demented non-Alzheimer-type patients and healthy control subjects. Using antibody P2-1 in an enzyme-linked immunosorbent assay, we measured CSF levels of APP in a larger population consisting of 13 patients diagnosed with probable AD, 18 patients diagnosed with dementia (non-Alzheimer type), and 16 nondemented, healthy controls. Mean CSF levels of APP were approximately 3.5-fold lower in the live patients diagnosed with probable AD compared to the demented non-Alzheimer-type controls or the nondemented, healthy individuals. These findings suggest that abnormal metabolism of APP is reflected in the extracellular fluids of the central nervous system and that CSF levels of soluble APP provide a useful biochemical marker to assist in the clinical diagnosis of AD.

Alzheimer Disease↗