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

It is currently believed that Parkinson disease (PD) is due to a degenerative process that independently damages multiple areas of the central and peripheral nervous system. Loss of nigrostriatal dopamine is now widely recognized as being directly related to the motor symptoms in Parkinson's disease. Parkinsonian patients also exhibit symptoms and signs suggestive of hypothalamic dysfunction (e.g. dysautonomia, impaired heat tolerance). The latter clinical features are supported by pathological, biochemical and endocrinological findings. Lewy body formation has been demonstrated in every nucleus of the hypothalamus, specifically the tuberomamillary and posterior hypothalamic. Preferential involvement of the hypothalamus was also noted in patients after post-encephalitic parkinsonism. Loss of dopamine (30-40%) in the hypothalamus of affected patients has been shown in recent studies, and is compatible with the reported abnormalities of growth hormone release in response to L-dopa administration, elevated plasma levels of MSH, and reduced CSF levels of somatostatin and beta-endorphins in these patients. Deranged immunological mechanisms have been found in PD patients including the presence of autoantibodies against sympathetic ganglia neurons, adrenal medulla and caudate nucleus. On the evidence of on pathological studies demonstrating the early vulnerability of the hypothalamus in aging and PD, and the known role of the hypothalamus in immune modulation, we expect that it will be shown that primary damage of the hypothalamus leads to subsequent secondary degeneration of structures receiving direct projections from the hypothalamus. Within this framework, the dopaminergic systems may be damaged, since striatal dopamine synthesis and receptor sensitivity have been shown to be regulated by ACTH and alpha-MSH through direct arcuate nucleus-striatal projections.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The hypothalamus in Parkinson disease. 288 37

We measured CSF and plasma contents of beta-endorphin (beta-EP), beta-lipotropin (beta-LPH), and ACTH in 24 patients with Parkinson's disease; 14 had not been treated. CSF beta-EP concentrations in untreated patients were lower than in 15 controls (p less than 0.005), but values did not differ significantly in treated and untreated patients. In untreated and treated patients, ACTH and beta-LPH CSF, and beta-EP, beta-LPH, and ACTH plasma concentrations were in the same range as controls. The Parkinson's disease-related decrease of CSF beta-EP levels further supports the concept that there is a generalized brain disorder in Parkinson's disease affecting more than dopaminergic neurons in the substantia nigra.
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PMID:beta-Endorphin cerebrospinal fluid decrease in untreated parkinsonian patients. 299 18

Electrophoretic studies of human CSF proteins from patients with diseases of the NS are reviewed. Various 1-DE methods are of similar value in identifying the non-specific OBs, which are helpful in the diagnosis of MS and recurrent GBS. In early and subclinical MS, OBs are of prognostic value, with IEF gels having the greater resolution. Silver-stained 2-DE gels provide the equivalent information to the OBs on 1-DE gels, with even greater sensitivity, and yield additional disease-associated protein data. Two proteins have proven to have diagnostic value in CJD and other changes that are still being evaluated have been identified in Parkinson's disease, GBS, Alzheimer's disease, schizophrenia and Herpes simplex encephalitis. The vastly improved CSF protein information obtained with silver-stained 2-DE gels heralds both a change from the relatively limited applications with 1-DE methods and also the need to adopt this approach in the routine clinical laboratory.
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PMID:Cerebrospinal fluid protein analysis in diseases of the nervous system. 306 25

In patients with Parkinson disease, improved visualization of brain iron on a mid-field-strength magnet can be obtained with T2-weighted images and elimination of phase-encoding artifacts. A long echo delay time accentuates the loss of signal from brain iron. However, the long pulse sequence creates phase-encoding artifacts from CSF pulsations at the level of the basal ganglia. These artifacts are eliminated and resolving power increased with additional pulsing in the slice-selective and read gradients. Elimination of motion artifacts enhances visualization of brain iron in three ways: (1) extrapyramidal nuclei containing iron have better definition, (2) abnormalities are better identified, and (3) pseudolesions disappear. Our findings suggest there is significant improvement in the resolving power of brain iron on MR scans made with a mid-field-strength scanner when gradient modification is used.
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PMID:Brain iron in patients with Parkinson disease: MR visualization using gradient modification. 312 74

CSF from Parkinson's disease (PD) patients undergoing autologous transplantation of adrenal medulla tissue into their lateral ventricle was examined for the presence of IgG. CSF from 6 of 7 patients incubated with rat brain tissue reacted immunocytochemically to neuronal cell bodies in the substantia nigra and ventral tegmental region. This reactivity gradually disappeared in the months following transplantation. Five of 6 CSF samples from non-transplanted PD patients also produced this immunocytochemical reactivity whereas 26 non-PD samples were immunonegative. Possible implications to the transplant procedure are discussed.
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PMID:An antibody in the CSF of Parkinson's disease patients disappears following adrenal medulla transplantation. 324 68

The possible involvement of dopaminergic neurons in dementia of Alzheimer type (AD/SDAT) was studied in autopsied brains from 20 patients with AD/SDAT. Dopamine (DA) concentrations were decreased significantly in the temporal cortex, hippocampal cortex and hippocampus in AD/SDAT patients. Levels of homovanillic acid (HVA) were not altered compared to controls. The HVA/DA ratio was significantly higher in the hippocampus of AD/SDAT patients, suggesting overactivity of the remaining DA neurons. Histological findings of substantia nigra suggesting coexistent pathology of Parkinson's disease (PD) found in 25% of cases were associated with lowered levels of DA in striatum and with reduced HVA in CSF. The activity of monoamine oxidase-B was significantly increased in the cortical areas and in the hippocampus, obviously reflecting the underlying cell loss and substantial gliosis in these areas of the brain. In general, DA neurons seemed to be only mildly involved in AD/SDAT. Coexistent PD pathology can explain the loss of DA in the striatum and the presence of clinical PD symptoms in some patients with AD/SDAT. Otherwise the clinical relevance of these dopaminergic alterations is unclear.
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PMID:Dopaminergic system and monoamine oxidase-B activity in Alzheimer's disease. 339 91

The CSF and sera of 7 patients with Parkinson's disease were investigated immunocytochemically, in order to see if antibodies were present which recognized DA-ergic cell bodies in glutaraldehyde fixed rat brain. In 2 patients a marked labeling of DA-ergic neurons in the substantia nigra was observed, identified by anti-DA antiserum and by 6-OHDA induced degeneration, but also other neurons in the ventral mesencephalon were recognized. The other patients were weakly positive or negative. Sera gave unspecific labelling of all neurons. In one patient the sub-classes of IgG were investigated and found to be of IgG3 (labeling nerve terminals) and of IgG1-2, low affinity type (recognizing perikarya). The epitopes recognized have not been identified, but are unlikely to be DA-like, since blocking experiments and ELISA-tests gave negative results. The possible clinical importance of the results are discussed.
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PMID:Immunocytochemical investigations on the presence of neuron-specific antibodies in the CSF of Parkinson's disease cases. 341 55

PPCE activity was found in human CSF by using a HPLC-fluorescence method. PPCE activity in CSF from control patients without neurological diseases was 2.19 +/- 0.78 (mean +/- SD) pmole (hr)-1.(ml)-1. PPCE activity in CSF from patients with Parkinson's disease was significantly decreased while PPCE activity in serum did not change significantly.
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PMID:Post-proline cleaving enzyme in human cerebrospinal fluid from control patients and parkinsonian patients. 348 Dec 69

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration is able to produce nigrostriatal damage and motor disabilities in primates similar to those seen in Parkinson's disease. Two months after MPTP treatment in African Green monkeys, significant depletions of dopamine (DA) and/or homovanillic acid (HVA) were found in the dorsal ventral tegmental area, and septum, but not in the ventral part of the ventral tegmental area or nucleus accumbens. However, DA losses were greater at all examined sites in the striatum. In putamen and caudate nucleus the decreases in DA and HVA appeared more marked dorsolaterally than ventromedially. After MPTP treatment the ratio HVA/DA was elevated in the septum and all striatal regions; in the striatum the increases in ratio were greater in the dorsolateral than in the ventromedial samples. NE concentration was not significantly altered by MPTP in the mesolimbic system. In control animals the HVA concentration and the ratio HVA/DA were higher in the putamen than in the caudate nucleus. A longitudinal study showed that CSF HVA and 3-methoxy-4-hydroxyphenylglycol were reduced by MPTP and remained below baseline level for 12 months after MPTP treatment. This biochemical study indicates that in the monkey MPTP is able to induce selective damage within both the nigrostriatal and mesolimbic DA systems.
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PMID:Effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on catecholamines and metabolites in primate brain and CSF. 349 38

By using a sensitive and specific method, DAP II activity was found in CSF. DAP II activity in CSF of control patients without neurological diseases was 0.416 +/- 0.141 (mean +/- SD) nmole/min/ml and was higher than DAP IV activity in CSF, 0.221 +/- 0.062 (mean +/- SD) nmole/min/ml. In contrast, DAP II activity in serum was 1.16 +/- 0.16 (mean +/- SD) nmole/min/ml and was lower than serum DAP IV activity [41.85 +/- 3.36 (mean +/- SD) nmole/min/ml]. This relatively high activity of DAP II in CSF compared with the activity of DAP IV in CSF together with recent histochemical evidence on the localization of DAP II in some neurons (7) suggests that CSF DAP II may be derived from the brain and may be a marker of some peptidergic neurons. DAP II activity in CSF of patients with Parkinson's disease was significantly increased, whereas DAP IV activity in CSF did not change significantly.
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PMID:Dipeptidyl-aminopeptidase II in human cerebrospinal fluid: changes in patients with Parkinson's disease. 360 98


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