Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hexose transporter protein of human erythrocyte membranes was investigated in aging and in demented patients with Alzheimer disease (AD) and Parkinson disease (PD) by assessing the D-glucose-displaceable binding of the ligand cytochalasin-B. We found no alteration in the hexose transporter of erythrocyte membranes in aging or in dementia of AD and PD. These findings indicate that the marked decrease in the density of hexose transporter that we previously reported in the cerebral cortex and brain microvessels in AD do not occur in erythrocyte membranes that have the highest density of the hexose transporter protein.
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PMID:The hexose transporter of human erythrocytes in aging and Alzheimer dementia. 259 23

In cases of Parkinson's disease, a high incidence of dementia and simultaneous pathologic changes of Alzheimer's type have been reported. X-ray CT and MRI have such good spatial resolution that they can be expected to be useful for evaluation of brain atrophy. Positron emission tomography (PET) used with 18F-2-deoxy-2-fluoro-D-glucose is considered to reflect regional function. By these techniques, brain atrophy and local cerebral metabolic rate of glucose (LCMR-glc) in patients with Parkinsonism with dementia was studied, and also compared with age-matched normal controls and senile dementia of Alzheimer type. In seven cases of Parkinson's disease with dementia, LCMRs-glc were statistically decreased in all regions in comparison with ten normal controls. LCMRs-glc in six Parkinson's disease without dementia were higher than those of demented Parkinson's disease, but significantly lower than normal controls in all regions except basal ganglia. Some aged normal controls presented cortical atrophy and a significant difference could not be seen in evaluation by MRI among these three groups. There was also no correlation between LCMR-glc and cortical atrophy. There was no significant difference of LCMR-glc between six Guamnian cases of Parkinsonism-Dementia complex (PD complex) without ALS and four cases of PD complex with ALS, and these values were significantly lower than five Guamanian and ten Caucasian normal controls. In PD complex with and without ALS, remarkable cortical atrophy and ventricular dilatation were recorded in comparison with normal controls, and correlation between decrement of LCMR-glc and cortical atrophy was indicated in frontal, parietal and temporal lobe. In Parkinson's disease with dementia and PD complex in Guam, LCMRs-glc in all regions of brain were generally lower than normal controls. These findings were different from Alzheimer's disease in which LCMR-glc have been reported to be low especially in cerebral cortex. On the other hand, cortical atrophy and ventricular dilatation evaluated by MRI and CT was apparent in PD complex, but these changes were not remarkable in Parkinson's disease. Cortical atrophy did not always correlate with the decrease of LCMR-glc and changes of LCMR-glc could reflect clinical signs such as Parkinsonism and dementia. Both PET as a functional imaging method and MRI, CT as an anatomical imaging method are useful to access the study of these diseases.
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PMID:[Comparison study of positron emission tomography, X-ray CT and MRI in parkinsonism with dementia]. 279 56

The in vitro effects of dopamine (DA) and insulin on -14C glucose oxidation (transport) in isolated rat adipocytes was studied. Low to intermediate concentrations of DA combined with low concentrations of insulin tended to stimulate glucose transport whilst high concentrations of DA combined with high concentrations of insulin produced inhibition of insulin stimulated glucose transport. The effect of DA on glucose transport was mediated via beta-adrenergic receptors, since propranolol, but not haloperidol or phentolamine, antagonised these effects of dopamine. These effects of dopamine on glucose transport may be relevant to the pathophysiology of Parkinson's disease and other neuropsychiatric conditions in which abnormalities of dopaminergic functions are thought to be of major pathogenic importance.
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PMID:Dopamine and insulin interact to modulate in vitro glucose transport in rat adipocytes. 306 82

Patterns of local cerebral glucose utilization were measured with positron emission CT using the 18F-fluorodeoxyglucose method in 13 patients with HD, 15 subjects at risk for HD, and control subjects. These data were compared with CT measures of cerebral atrophy, age, and duration and severity of symptoms. The results indicate that in HD there is a characteristic decrease in glucose utilization in the caudate and putamen and that this local hypometabolism appears early and precedes bulk tissue loss. In contrast to demented patients with Alzheimer's disease or Parkinson's disease, in these HD patients glucose utilization typically was normal throughout the rest of the brain, regardless of the severity of symptoms and despite apparent shrinkage of brain tissue. Our results indicate that the caudate is hypometabolic in some asymptomatic persons who are carriers of the autosomal-dominant gene for HD.
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PMID:Local cerebral glucose utilization in symptomatic and presymptomatic Huntington's disease. 316 Nov 65

The quantitative autoradiographic 2-[14C]deoxyglucose method was used to map the distribution of alterations of local cerebral metabolic rate for glucose (lCMRGlc) in the oculomotor system of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-(MPTP)-induced parkinsonian monkeys. The lCMRGlc was decreased in the frontal eye fields and in the paralamellar mediodorsal thalamus in the parkinsonian monkeys as compared to normal controls. No changes in lCMRGlc were observed in other areas of the oculomotor system. L-Dopa therapy reversed the oculomotor symptoms in these monkeys, as well as the decrease of lCMRGlc in the frontal eye fields and the paralamellar mediodorsal thalamus. Because the frontal eye fields are known to be involved in the initiation of voluntary saccades, these findings suggest a functional anatomical basis for the oculomotor deficits in Parkinson's disease.
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PMID:Metabolic mapping of the oculomotor system in MPTP-induced parkinsonian monkeys. 325 55

The quantitative 2-[14C]deoxyglucose autoradiographic method was used to map the pattern of alterations in local cerebral glucose utilization associated with the Parkinsonian syndrome induced by the administration of the neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), to rhesus monkeys. Monkeys treated with the neurotoxin exhibited both behavioral symptoms (e.g. akinesia, rigidity, flexed posture, and eyelid closure) and neuropathological changes (degeneration of the cells of the substantia nigra pars compacta) that closely paralleled those in human Parkinson's disease. Glucose utilization was significantly reduced in the pars compacta of the substantia nigra and in the subthalamus, and increased in the external segment of the globus pallidus. Outside the basal ganglia reductions in glucose utilization were limited to the mediodorsal nucleus of the thalamus, frontal eye fields, and ventral tegmental area. The results of these studies indicate that the profound functional and behavioral deficits in MPTP-induced Parkinson's syndrome are the consequences of highly selective functional changes in a few cerebral structures, mainly within the basal ganglia.
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PMID:Changes in local cerebral glucose utilization associated with Parkinson's syndrome induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in the primate. 349 79

Nine adult monkeys (Macaca fascicularis) were used in this study. Five animals were used as controls. Three animals were injected intravenously daily with 0.5 mg/kg of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) over a 4-day period; one animal was injected weekly over a 4-week period. Neurological examination of the MPTP-treated animals revealed a flexed posture of trunk and extremities, bradykinesia, increased tone without cogwheel rigidity, loss of vestibular righting reflexes, decreased vocalization and swallowing, failure of upgaze and abnormal pursuit eye movements. Reflexes were hyperactive. The compound 2-deoxy-D-[14C]glucose (2-DG) was utilized for the determination of the local cerebral metabolic rate for glucose (lCMRg). A generalized decrease in lCMRg was noted in all cerebral cortical areas as compared to control values. The cerebellar cortex demonstrated no change in lCMRg. Areas that demonstrated a significant increase in lCMRg were: the internal and external segments of the globus pallidus (P less than 0.01), the pars compacta and the pars reticulata of the substantia nigra (P less than 0.05). Areas that demonstrated a significant decrease in lCMRg were: the head of the caudate nucleus (P less than 0.05), the anterior dorsomedial putamen (P less than 0.05) and the anterior segment of the subthalamic nucleus (P less than 0.05). The 2-DG analysis of the MPTP primate model of Parkinson's disease is particularly suited to demonstrate areas in the central nervous system that are affected by this neurotoxin. Further studies of these areas may lead to a better understanding of the mechanisms that underlie the clinical symptomatology of Parkinson's disease.
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PMID:Changes in the local cerebral metabolic rate for glucose in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) primate model of Parkinson's disease. 387 82

Patterns of local cerebral glucose utilization were measured with positron emission tomography using the fluorine-18-labeled fluorodeoxyglucose (18FDG) method in 8 patients with Parkinson's disease, in 13 patients with Huntington's disease, in 15 subjects at risk for Huntington's disease, and in aged-matched normal control subjects. On the average, global cerebral metabolism in patients with Parkinson's disease was moderately reduced (20%), but the relative distribution of glucose utilization throughout the brain in these patients was normal. These results support the conclusion that alterations of the nigrostriatal pathway in Parkinson's disease have no major selective effect on the metabolism of particular cerebral regions. In Huntington's disease, however, there was a characteristic decrease in glucose utilization in the caudate nuclei and putamen, and this local hypometabolism appeared early and preceded bulk tissue loss. In patients with Huntington's disease, glucose utilization typically was normal throughout the rest of the brain, regardless of the severity of symptoms and despite the apparent shrinkage of brain tissue. The results also suggest the possibility that the caudate nuclei may be hypometabolic in some asymptomatic subjects who are potential carriers of the autosomal dominant gene for Huntington's disease.
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PMID:Patterns of cerebral glucose utilization in Parkinson's disease and Huntington's disease. 623 56

Using the 18f-fluoro-2-deoxy-d-glucose technique and positron emission tomography (PET), the local cerebral glucose utilisation (1CMRGlc) was measured in four non-demented patients with early-onset, bilateral Parkinson's disease characterised by the predominance of akinesia. The study was done twice, first in the untreated condition, and then after levodopa had been resumed. Despite a marked clinical improvement, we found no alteration in 1CMRGlc between the first and second studies in any of the brain structure analysed. Compared to control values, 1CMRGlc in the basal ganglia was moderately increased in both studies. These essentially negative findings agree with most previous human or animal studies, and indicate that the functional alterations in the central dopaminergic systems of patients with Parkinson's disease have metabolic correlates that are too small to be demonstrated by current PET devices.
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PMID:Local cerebral glucose utilisation in treated and untreated patients with Parkinson's disease. 633 76

Acutely administered caffeine modestly increases blood pressure, plasma catecholamine levels, plasma renin activity, serum free fatty acid levels, urine production, and gastric acid secretion. It alters the electroencephalographic spectrum, mood, and sleep patterns of normal volunteers. Chronic caffeine consumption has no effect on blood pressure, plasma catecholamine levels, plasma renin activity, serum cholesterol concentration, blood glucose levels, or urine production. Caffeine does not appear to be useful for increasing the motility of hypomotile sperm in artificial insemination or in the therapy of minimal brain dysfunction, cancer, or Parkinson's syndrome, but it may be effective as a topical treatment of atopic dermatitis and as systemic therapy for neonatal apnea. Caffeine does not seem to be associated with myocardial infarction; lower urinary tract, renal, or pancreatic cancer; teratogenicity; or fibrocystic breast disease. The role of caffeine in the production of cardiac arrhythmias or gastric or duodenal ulcers remains uncertain.
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PMID:The health consequences of caffeine. 634 91


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