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)

The micro-architecture of the substantia nigra was studied in control cases of varying age and patients with parkinsonism. A single 7 mu section stained with haematoxylin and eosin was examined at a specific level within the caudal nigra using strict criteria. The pars compacta was divided into a ventral and a dorsal tier, and each tier was further subdivided into 3 regions. In 36 control cases there was a linear fallout of pigmented neurons with advancing age in the pars compacta of the caudal substantia nigra at a rate of 4.7% per decade. Regionally, the lateral ventral tier was relatively spared (2.1% loss per decade) compared with the medial ventral tier (5.4%) and the dorsal tier (6.9%). In 20 Parkinson's disease (PD) cases of varying disease duration there was an exponential loss of pigmented neurons with a 45% loss in the first decade. Regionally, the pattern was opposite to ageing. Loss was greatest in the lateral ventral tier (average loss 91%) followed by the medial ventral tier (71%) and the dorsal tier (56%). The presymptomatic phase of PD from the onset of neuronal loss was estimated to be about 5 yrs. This phase is represented by incidental Lewy body cases: individuals who die without clinical signs of PD or dementia, but who are found to have Lewy bodies at post-mortem. In 7 cases cell loss was confined to the lateral ventral tier (average loss 52%) congruent with the lateral ventral selectivity of symptomatic PD. It was calculated that at the onset of symptoms there was a 68% cell loss in the lateral ventral tier and a 48% loss in the caudal nigra as a whole. The regional selectivity of PD is relatively specific. In 15 cases of striatonigral degeneration the distribution of cell loss was similar, but the loss in the dorsal tier was greater than PD by 21%. In 14 cases of Steele-Richardson-Olszewski syndrome (SRO) there was no predilection for the lateral ventral tier, but a tendency to involve the medial nigra and spare the lateral. These findings suggest that age-related attrition of pigmented nigral cells is not an important factor in the pathogenesis of PD.
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PMID:Ageing and Parkinson's disease: substantia nigra regional selectivity. 193 45

It is known that progressive supranuclear palsy (PSP) shows subcortical dementia. The diagnosis of PSP is sometimes difficult because this disorder mimics the clinical features of parkinsonian syndrome. Several PET studies demonstrated frontal hypo-metabolism in PSP patients. We studied the cerebral blood flow (CBF) pattern by single-photon-emission-computed tomography (SPECT) using 123I-isopropyl-iodoamphetamine (IMP) in 5 patients of PSP including one autopsy case. Five PSP patients were 3 men and 2 women, mean age of 67.6 years old. Control groups were 3 normal controls (Normal), 7 patients of Parkinson's disease (PD), 5 patients of olive-pontocerebellar atrophy (OPCA), and 4 patients of dementia of Alzheimer's type (DAT). CBF was measured by 123I-IMP SPECT using 400 AC/T Starcam (GE). CBF was measured by semi-quantitative methods. Regions of Interest (ROI's) were located at cerebellar, basal ganglion, and lateral ventricle levels. Each count of ROI was divided by the count of occipital ROI. In all PSP patients, the ratio of relative blood flow to occipital lobe in the frontal and fronto-temporal regions were most markedly affected, showing average reduction rates of 66.6% and 65.5%. These rates showed statistically significant differences to other control degenerative neurological diseases. Our these results correspond to the former PET studies. Moreover, frontal hypoperfusion progressed with advancing clinical stage. The results indicate that CBF study with SPECT is useful to confirm the diagnosis of PSP. It is necessary to clarify the role of the damage in basal ganglia for frontal hypometabolic pattern.
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PMID:[Cerebral blood flow pattern in progressive supranuclear palsy]. 193 73

The technique of receptor autoradiography was used to study the distribution of neurotensin receptors in post mortem brain tissues from patients affected by Parkinson's disease, progressive supranuclear palsy and from age-matched controls. [125I]Neurotensin was used as ligand. Significant receptor decreases were found in the substantia nigra, both pars compacta and reticulata, and in the putamen in Parkinson's disease and progressive supranuclear palsy. In addition, significant decreases of neurotensin receptors were found in the ventral tegmental area, nucleus accumbens and dorsal part of caudate head in patients with Parkinson's disease but not in patients with progressive supranuclear palsy, indicating differential involvement of neurotensin receptors in these two neurological disorders. In addition, both in Parkinson's disease and progressive supranuclear palsy the decrement of striatal neurotensin binding sites was less than expected from the reported decrease of dopamine content in this nucleus, suggesting only partial localization of neurotensin receptors on mesostriatal dopaminergic projections.
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PMID:Neurotensin receptors in Parkinson's disease and progressive supranuclear palsy: an autoradiographic study in basal ganglia. 196 15

We investigated tyrosine-hydroxylase (TH)-immunoreactive neurons in the medulla oblongata corresponding to the A1 and A2 cell groups in autopsy tissue of patients with Parkinson's disease (PD) (n = 3), progressive supranuclear palsy (PSP) (n = 3), striatonigral degeneration (SND) (n = 2), and in controls (n = 4). The estimated total number of TH-positive neurons in the A1 and the A2 regions was normal in PD and PSP patients. The sparing of medullary catecholaminergic cells in PD and PSP may be related to their minor degree of melanization and the possibility that intermediate compounds associated with the oxidative catabolism of norepinephrine and epinephrine may be less cytotoxic than those generated by degradation of dopamine. Patients with SND showed a marked loss of TH-immunoreactive cells in the A1 and the A2 groups, which may contribute to the impairment of vasomotor control characteristic of the disease.
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PMID:Catecholaminergic systems in the medulla oblongata in parkinsonian syndromes: a quantitative immunohistochemical study in Parkinson's disease, progressive supranuclear palsy, and striatonigral degeneration. 197 60

The levels of different elements were studied by x-ray microanalysis in the substantia nigra and the central gray substance of patients with Parkinson's disease, progressive supranuclear palsy, and matched controls. In control brains, only iron, potassium, silicum, sodium, sulfur, and zinc were within the limit of detection of the technique. The abundance of each element was different, but their respective concentrations in the two brain regions were similar, except for sulfur levels which were higher on neuromelanin aggregates in the substantia nigra than in nigral regions lacking neuromelanin, and in the central gray substance. In Parkinson's disease, but not in progressive supranuclear palsy, nigral iron levels increased in regions devoid of neuromelanin and decreased on neuromelanin aggregates, but were unchanged in the central gray substance, when compared to control values. Concentrations of the other elements in the central gray substance and substantia nigra were not different from controls in brains from patients with Parkinson's disease and progressive supranuclear palsy. Analysis of Lewy bodies in the parkinsonian substantia nigra revealed high levels of iron and the presence of aluminum. Metal abundance was not affected in progressive supranuclear palsy, in spite of the nigral cell death. This suggests that the increased iron levels and the detection of aluminum observed in Parkinson's disease are not solely the consequence of the neuronal degeneration.
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PMID:Iron and aluminum increase in the substantia nigra of patients with Parkinson's disease: an X-ray microanalysis. 198 48

To determine the possible role of Wallerian degeneration secondary to the grey matter neuronal loss in the pathogenesis of "leuko-araiosis", computerised tomography (CT) of the brain was studied in 98 normotensive and non diabetic subjects free of cardiac diseases: 32 with Alzheimer's disease, 36 with Parkinson's disease, eight with progressive supranuclear palsy, and 22 controls. In Alzheimer's disease, leuko-araiosis scores were greater than in control subjects. Leuko-araiosis was more prominent in anterior periventricular areas in Parkinson's disease and progressive supranuclear palsy, and in posterior periventricular areas in Alzheimer's disease. In two patients with Alzheimer's disease and leuko-araiosis, necropsy revealed diffuse white matter pallor, mild fibrillary astrocytosis, and in one patient limited hyaline thickening of small white matter vessels, without any infarction or hypertensive change. Changes were more severe in white matter close to cortical areas with a great density of neurofibrillary tangles. Leuko-araiosis was more severe or more widespread in Alzheimer's disease than in Parkinson's disease, progressive supranuclear palsy and normal ageing. Differences in the location of leuko-araiosis between the four groups might be due to differences in the location of the grey matter disorder and Wallerian degeneration rather than amyloid in Alzheimer's disease, Parkinson's disease, progressive supranuclear palsy and normal ageing. Wallerian degeneration might be another cause of leuko-araiosis in neuro-degenerative disorders beside previously reported extra-cerebral predisposing factors and amyloid angiopathy.
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PMID:Could Wallerian degeneration contribute to "leuko-araiosis" in subjects free of any vascular disorder? 201 Jul 59

Regional cerebral perfusion was evaluated by single photon emission computed tomography (SPET) using technetium 99m hexamethylpropylene amine oxime (99mTc-HMPAO) as a tracer, in 13 control subjects and 44 age-matched patients suffering from dementia of the Alzheimer's type (DAT, n = 19), presumed Pick's disease (n = 5), idiopathic Parkinson's disease with dementia (DPD, n = 15) and progressive supranuclear palsy (PSP, n = 5). HMPAO uptake was measured in the superior frontal, inferior frontal, parietal, temporal and occipital cortices, and the perfusion values were expressed as cortical/cerebellar activity ratios. As compared with controls, tracer uptake ratios in the DAT group were significantly reduced over all cortical regions, with the largest defects in the parieto-temporal and superior frontal cortices. A marked hypoperfusion affecting the superior and inferior frontal cortices was found in Pick's disease, whereas a mild but significant hypoperfusion was observed only in the superior frontal cortex of patients with PSP. In the DPD group, HMPAO uptake was significantly reduced in the parietal, temporal and occipital cortices, but not in the frontal cortex. These results show that DAT and DPD share an opposite anteroposterior HMPAO uptake defect as compared with the Pick's and PSP groups.
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PMID:A comparative technetium 99m hexamethylpropylene amine oxime SPET study in different types of dementia. 201 79

Olfactory dysfunction is among the first signs of Alzheimer's disease (AD), idiopathic Parkinson's disease (PD), and the parkinsonism-dementia complex (PDC) of Guam. We have recently demonstrated that the odor identification and detection deficits of patients with PD are equivalent to those of patients with mild AD when subtle differences in cognitive function are statistically controlled for by analysis of covariance. In contrast, patients with progressive supranuclear palsy (PSP) and patients with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism evidence olfactory function much more similar to that of normal controls. In the present study, we administered the University of Pennsylvania Smell Identification Test and the Picture Identification Test to 24 patients with early signs of the PDC of Guam and statistically compared their test scores to those of 24 early-stage AD and 24 early-stage PD patients of similar age and gender from the United States mainland. Although the PDC group evidenced slightly more difficulty in identifying pictures than did the other 2 groups, the odor identification deficit associated with this disorder was of the same magnitude as that observed in AD and PD, suggesting that olfactory testing cannot be used to distinguish among these 3 diseases and that the olfactory dysfunction of these disorders may reflect a common neurologic substrate.
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PMID:Odor identification deficit of the parkinsonism-dementia complex of Guam: equivalence to that of Alzheimer's and idiopathic Parkinson's disease. 204 98

Research into the cellular changes in the degenerative diseases of the central nervous system has focused on the alterations in the constituent proteins of the neuronal cytoskeleton. Although both microtubule and neurofilament proteins have been implicated in the formation of neurofibrillary pathology in Alzheimer, Pick, diffuse Lewy body and Parkinson diseases and progressive supranuclear palsy (PSP), until recently there has been little consideration of whether other cytoskeletal systems are involved. With the findings that epitopes of the microfilament associated protein tropomyosin are present in the neurofibrillary pathology of Alzheimer disease, we decided to investigate the presence of this protein in these related diseases. To address whether the inclusion bodies of other degenerative diseases share this property, sections of brain were immunostained with antibodies to smooth and skeletal muscle tropomyosin. Although neurofibrillary tangles in PSP, Pick bodies and some diffuse Lewy bodies stained, Lewy bodies of idiopathic Parkinson disease did not. This property further distinguishes the Lewy body of Parkinson disease from other neurofibrillary pathologies.
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PMID:Tropomyosin distinguishes Lewy bodies of Parkinson disease from other neurofibrillary pathology. 205 46

We present a clinical study of a patient aged 69 years with a clinical history of severe difficulty in walking and voluntary conjugate eye movement reduction in sideways glance and absence in vertical gaze. These symptoms led to diagnosis of Parkinson disease and treatment with L-Dopa + anticholinergics drugs. The treatment with antiparkinsonian drugs was suspended and no change in his clinical condition resulted. Methysergide therapy was initiated and the patient's response was monitored by video recording. On the basis of our experience and the data reported in the literature we believe that methysergide therapy affords some relief of symptoms in patients suffering from PSP.
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PMID:Treatment of progressive supranuclear palsy with methysergide. A clinical study. 207 61


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