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)

In 9 patients with progressive supranuclear palsy and in 27 controls, dopamine and homovanillic acid concentrations, choline acetyltransferase (CAT) activity, and the number of [3H]spiperone and [3H]quinuclidinyl benzilate binding sites were measured post mortem in the striatum (caudate nucleus, putamen, and nucleus accumbens), substantia innominata, and frontal cortex. Dopamine and homovanillic acid concentrations were reduced in the caudate nucleus and putamen but not in the nucleus accumbens or frontal cortex, indicating that the nigrostriatal dopaminergic system is lesioned in patients with progressive supranuclear palsy (as in those with Parkinson's disease) but not the mesocortical and mesolimbic dopaminergic systems, which are lesioned in parkinsonian patients. CAT activity and [3H]spiperone binding decreased in parallel fashion in all the structures. In the striatum, this suggests that the cholinergic neurons, which are target cells of the nigrostriatal system, also degenerate in this disease. This might explain the decrease in the number of dopamine receptors as well as the inefficacy of levodopa or anticholinergic therapy in these patients. The decrease in CAT activity in the substantia innominata and the frontal cortex indicates that the innominatocortical cholinergic system is lesioned in patients with progressive supranuclear palsy and may play a role in the intellectual deterioration observed. This lesion is also found in demented patients with Alzheimer's and Parkinson's diseases.
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PMID:Dopaminergic and cholinergic lesions in progressive supranuclear palsy. 300 Feb 80

An autopsy case is reported which revealed not only clinical and neuropathological features of progressive supranuclear palsy, but also the presence of large numbers of Lewy bodies in the brain stem nuclei and cerebral cortex. This case seems to be progressive supranuclear palsy with Lewy bodies distributed as in Parkinson's disease. Such case has not been previously reported.
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PMID:Progressive supranuclear palsy with Lewy bodies. 302 36

Mabs directed against phosphorylated epitopes on the heavy and medium neurofilament protein were used to immunostain histological sections from brains of patients without neurological disease and patients suffering from SDAT, Pick's disease, Parkinson's disease, progressive supranuclear palsy and encephalomalacias of the white matter inducing chromatolysis in the overlying cortex. In normal brains only axons but never perikarya were stained. In the pathological brains, however, swollen neurons with chromatolysis and swollen cells in Pick's disease, NFT in SDAT, Pick bodies in Pick's disease, the centers of Lewy bodies in Parkinson's disease and some tangles in progressive supranuclear palsy were stained. These changes are perikaryal alterations. The results are discussed in relation to the formation of NFT in SDAT, i.e. the PHF as seen by electron microscopy. It is concluded that in spite of the reliable staining of NFT with some of our mabs, with sera directed against PHF, MAPs and other cytoskeletal proteins there is no absolutely specific immunoreaction for PHF. The most similar pattern to that observed in NFTs of SDAT is seen in the Pick bodies of Pick's disease, although these do not consist of PHF when looked at with the electron microscope, and although they behave differently from NFT in some 'conventional' histological stains. From this nonspecificity of the immunoreaction and from the presence of multiple cytoskeletal epitopes in NFT it is concluded that NFT (i.e. PHF) are probably not derived from one particular cytoskeletal element but are reassembled from proteolytic breakdown fragments of several of these elements. In this regard the similarities and dissimilarities with the alterations of Pick's disease might be specially relevant and deserve further studies, especially as the clinical features of SDAT and Pick's disease can be very similar.
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PMID:Cytoskeletal immunohistochemistry of Alzheimer's dementia and related diseases. A study with monoclonal antibodies. 312 6

To investigate central processing time in patients with progressive supranuclear palsy and Parkinson's disease, reaction times were measured using tasks with different levels of cognitive complexity but with the same motor response. In patients with Parkinson's disease, the additional central processing time required for more complex situations was no different from that in control subjects, suggesting that cognitive aspects of the reaction time procedures tested were possibly too simple to reveal a slowing of thought processes in these patients. Conversely, the central processing time was increased in patients with progressive supranuclear palsy compared with both Parkinson's disease and control subjects. The increase was associated with impairment in frontal lobe test performance. These results confirm that a slowing of central processing is a prominent feature of the cognitive disturbances of progressive supranuclear palsy and, furthermore, suggest that this slowing may be related to striatofrontal dysfunction.
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PMID:Slowing of cognitive processing in progressive supranuclear palsy. A comparison with Parkinson's disease. 319 Apr 99

The number of serotonin-S2 receptors was decreased in the temporal cortex of patients with Parkinson's disease and progressive supranuclear palsy (PSP). There was no significant modification of these receptors in the frontal cortex or in the hippocampus and putamen in both diseases. The decrease in number of receptors in PSP was unexpected, because the cerebral cortex is thought to be spared in this disease. There was no correlation between the decrease in number of serotonin-S2 receptors and the degree of dementia in Parkinson's disease, suggesting that these receptors are not directly involved in the deterioration of cognitive functions.
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PMID:Decrease of serotonin-S2 receptors in temporal cortex of patients with Parkinson's disease and progressive supranuclear palsy. 319 63

Leukocyte glutamate dehydrogenase (GDH) activity was measured in 39 normal subjects, 32 neurological controls, 66 patients with progressive ataxic disorders, 32 with multiple system atrophy, 40 with Parkinson's disease, eight with Steele-Richardson-Olszewski syndrome, eight with juvenile Parkinsonism and four with the dystonia-Parkinsonism syndrome. GDH activity was reproducible to within 10% in leukocyte pellets stored at -70 degrees C for up to 9 months, and did not vary with sex or age in control subjects. There was marked variation in the relative proportions of heat stable and heat labile forms of GDH between control subjects and on repeated assay in the same subject. Total leukocyte GDH activity was similar in normal subjects and neurological controls. Mean total GDH activity was reduced in all patient groups by between 15 to 29% compared with controls. Fourteen patients had total GDH activity below 50% of the control mean, but low values were not specific for any one disease (five had ataxic disorders, four Parkinson's disease, three multiple system atrophy, one juvenile Parkinsonism, and one dystonia-Parkinsonism). The heat labile fraction of GDH represented about 20% of total activity in control subjects, and 27% in the patients with reduced total GDH activity. Thus low GDH activity was not disease-specific in this study, and the heat-labile GDH fraction was not selectively affected. "Reduced" leucocyte GDH activity in some patients may represent no more than the lower end of a normal distribution.
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PMID:Leukocyte glutamate dehydrogenase activity in patients with degenerative neurological disorders. 320 97

[3H]GBR 12935 bound with high affinity to dopamine uptake sites in rat striatum where a close parallelism was observed between the subcellular localization profiles for [3H]dopamine uptake and [3H]GBR 12935 specific binding. Using the same ligand, we characterized the dopamine uptake sites in human striatum: the mean KD value was 3.2 nM and the specific binding was inhibited by several dopamine uptake blockers but with slightly lower affinities than those observed in the rat. The subcellular localization profile revealed a synaptosomal enrichment of the specific binding in human striatum. [3H]GBR 12935 binding was decreased in the putamen and caudate nucleus of subjects with Parkinson's disease (33 and 46% of control values, respectively) and progressive supranuclear palsy (38 and 57% of control values, respectively). It is very unlikely that the remaining binding sites in both diseases correspond to piperazine acceptor sites that are not involved in dopamine uptake. However, we cannot exclude the possibility that some of these remaining dopamine transporter sites are not functional, since the reduction in [3H]GBR 12935 specific binding was less marked than the decrease in the dopamine content of the same areas.
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PMID:[3H]GBR 12935 binding to dopamine uptake sites: subcellular localization and reduction in Parkinson's disease and progressive supranuclear palsy. 321 81

Subcortical dementia occurs both in disorders affecting the basal ganglia (for example, Parkinson's disease, Huntington's disease, and progressive supranuclear palsy) and in a variety of subcortical vascular, infectious, inflammatory, neoplastic, and traumatic conditions. The principal features of subcortical dementia include bradyphrenia, impairment of executive function, recall abnormalities, visuospatial disturbances, depression, and apathy. The syndrome contrasts with dementia of the Alzheimer type in which cortical involvement produces aphasia, combined recall and recognition deficits, and indifference. Electrophysiologic, biochemical, and metabolic studies support a distinction between subcortical and cortical dementias.
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PMID:Psychological dysfunction accompanying subcortical dementias. 328 89

Two antigens, G7 and G9, which are labelled by monoclonal antibodies in Lewy bodies in brains from patients with Parkinson's disease, were characterized by two-dimensional electrophoresis, followed by electroblotting, in order to explore their possible relationship with neuronal degeneration in this disease. The G7 antigen was found in the substantia nigra of subjects with Parkinson's disease and progressive supranuclear palsy, as well as in normal subjects. It was also found in the dopaminergic nucleus paranigralis and the locus coeruleus. The G9 antigen was found in the substantia nigra and locus coeruleus, but also in the caudate nucleus, terminal region of the nigrostriatal dopaminergic neurons, and in the cortex and cerebellum, terminal regions of the noradrenergic neurons in the locus coeruleus. The identity of the antigens remains unknown. They do not correspond to tyrosine hydroxylase or neurofilaments previously detected in Lewy bodies, or to other cytoskeletal proteins. Nor are they related to the presence of neuromelanin in the cells that degenerate in Parkinson's disease. The proteins, or at least the epitopes labelled by the antibodies, are found in normal brain, suggesting that these proteins do not play a causal role in the formation of the Lewy bodies in degenerating neurons in Parkinson's disease. The G7 antigen is absent from the cholinergic substantia innominata, where Lewy bodies are also found, indicating that these antigens are not essential for the formation of the corpuscle.
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PMID:Characterization of two antigens in parkinsonian Lewy bodies. 335 27

We measured amino acid contents in autopsied brains of seven patients with progressive supranuclear palsy (PSP) and in control subjects dying without brain disease. Glutathione was also quantitated in rapidly frozen brains of PSP patients, Parkinson's disease (PD) patients, and controls. In PSP, we found glutamic acid markedly increased in the nucleus accumbens; taurine significantly increased in nucleus accumbens, substantia nigra, and globus pallidus; and gamma-aminobutyric acid significantly increased in nucleus accumbens and putamen. Glycerophosphoethanolamine contents were significantly increased in most regions. Glutathione, which is significantly decreased in substantia nigra in PD, was increased in this brain region in PSP, suggesting that different mechanisms may be responsible for destruction of dopaminergic nigrostriatal neurons in these two disorders.
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PMID:Brain amino acids and glutathione in progressive supranuclear palsy. 336 77


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