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 binding of the selective 5-HT2 antagonist [3H]ketanserin has been investigated in the temporal cortex of patients with Alzheimer's disease (SDAT), Parkinson's disease (PD), senile dementia of Lewy body type (SDLT) and neuropathologically normal subjects (control). 5-HT2 binding was reduced in SDAT, PD with dementia and SDLT. SDAT showed a 5-HT2 receptor deficit across most of the cortical layers. A significant decrease in 5-HT2 binding in the deep cortical layers was found in those SDLT cases without hallucinations. SDLT cases with hallucinations only showed a deficit in one upper layer. There was a significant difference in cortical layers III and V between SDLT without hallucinations and SDLT with hallucinations. The results confirm an abnormality of serotonin binding in various forms of dementia and suggest that preservation of 5-HT2 receptor in the temporal cortex may differentiate hallucinating from non-hallucinating cases of SDLT.
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PMID:Cortical serotonin-S2 receptor binding in Lewy body dementia, Alzheimer's and Parkinson's diseases. 177 39

Harding et al. suggested at first that an increase of P2 latency in flash VEP without an increase of P2 latency in pattern reversal VEP may be a diagnostic marker of Alzheimer's disease. Up to now there is no convincing evidence for this hypothesis. The purpose of the present study was to examine this hypotheses in an extended group of patients with Alzheimer's disease (n = 36). In addition, a group of patients with Parkinson's disease (n = 8) without dementia syndrome and a group of healthy elderly controls (n = 46) was investigated in order to determine the sensitivity and specificity of these VEP parameters. The results confirmed significant group differences between patients with Alzheimer's disease and healthy controls concerning the increase of Flash P2 latency and unchanged latency of P2 in the pattern reversal VEP. No significant correlations were found between duration of illness and mental test scores. The group differences of P2 latency in the flash VEP for patients with Parkinson's disease and healthy controls were also significant. Therefore, the increase of flash P2 latency in VEP does not seem to be specific for Alzheimer's disease nor for dementia syndrome. The pathological mechanism causing the flash P2 latency increase in a remarkable number of neuropsychiatric patients should be elucidated in further experimental investigations.
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PMID:[Visual evoked potentials in Alzheimer's and Parkinson disease]. 178 86

We compared the muscarinic cholinergic binding in lymphocytes of 44 patients with idiopathic Parkinson's disease with 23 age-matched normal volunteers, using [3H]quinuclidinyl benzilate. In 24 patients with Parkinson's disease without dementia, binding was normal in 12, below control values in 6, whereas the remaining 6 (all on anticholinergic medication) showed very high binding. In all 20 patients with Parkinson's disease and with dementia, the binding was below control levels, indicating that in these patients, as in patients with Alzheimer's dementia, the cholinergic muscarinic binding by lymphocytes is reduced.
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PMID:Changes of muscarinic cholinergic binding by lymphocytes in Parkinson's disease with and without dementia. 178 98

Regional cerebral blood flow (CBF) was examined in 27 patients with Parkinson's disease using single-photon emission computed tomography and N-isopropyl-p-[123I]iodoamphetamine as a tracer. Their CBF pattern was compared with that of seven patients with Alzheimer's disease and nine age-matched neurologically normal controls. Tracer activity was determined in seven bilateral cerebellar, cortical, and subcortical regions and was expressed as the ratio of activity in each region to the mean tracer activity in the cerebellar region. Nineteen patients with nondemented Parkinson's disease showed significantly decreased tracer activity ratio in the frontal and temporal cortices, basal ganglia, and thalamus compared with that in controls. The eight demented Parkinson's disease patients showed significantly decreased tracer activity ratio in the temporal and parietal cortices compared with the patients without dementia, and demonstrated CBF pattern similar to that of patients with Alzheimer's disease. These findings suggest that in patients with Parkinson's disease, the mechanism of CBF reduction of the frontal cortical region differs from that in the temporoparietal cortical region and support the concept that Parkinson's disease and Alzheimer's disease may overlap in some patients.
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PMID:Cerebral blood flow and dementia in Parkinson's disease. 178 7

Parkinson's disease (PD) is often associated with dementia in elderly patients, and sometimes PD coexists with senile dementia of the Alzheimer type (SDAT) or cerebrovascular disease (CVD) in the elderly. However, since there are few previous clinical studies on the coincidence of, or relationship between PD and CVD, the authors evaluated these aspects in 34 elderly patients with PD using MRI and SPECT. All the patients were over 70 years old. The diagnosis of PD was based on the presence of three symptoms (resting tremor, cogwheel rigidity and bradikinesia) which are characteristic of PD, and the effectiveness of L-DOPA therapy. We therefore believe that patients with vascular Parkinsonism were excluded from our study. In 34 cases, 24 (71%) had MRI evidence of CVD (mainly the lacunar state). In the 10 cases who had no CVD, 2 (20%) had severe dementia and the decrease of regional cerebral blood flow (rCBF) in the temporal and parietal lobes bilaterally correlated with the SPECT findings commonly found in SDAT. A comparison of the rCBF and the results of Hasegawa's dementia score (HDS) (verbal intelligence score) was made between the patients with PD associated with CVD and the patients with PD who had no CVD and no SPECT findings which correlated with SDAT. The rCBF in the frontal lobes and the results of the HDS of the former group were significantly lower than those of the latter. As mentioned above, elderly patients with PD often had CVD, leading to dementia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A clinical study in elderly patients with Parkinson's disease using MRI and SPECT--Parkinson's disease and the lacunar state]. 179 37

Event-related potentials (ERPs) occurring in response to attended and unattended stimuli were studied in 31 patients with Parkinson's disease (mean age: 66.9 years), 9 patients with Alzheimer's disease (mean age: 73.6 years) and 37 normal subjects (mean age: 47.5 years). Of the 31 patients with Parkinson's disease, 6 met the criteria for dementia in DSM-III-R. ERPs were recorded during the performance of visual discrimination tasks using three kinds of stimuli: frequent non-target (62%), infrequent non-target (19%) and infrequent target (19%) stimuli. The P3a and P3b were identified as the components of the P3 (P300) responses to infrequent non-target stimuli and infrequent target stimuli. Both the P3a and P3b latencies were significantly prolonged with normal aging. Nine of the Parkinson's disease patients showed a P3b latency above the 95% confidence limit of the age estimated regression line, while only one patient showed a prolonged P3a latency. There was no significant correlation between the P3a and P3b latencies in the patients with Parkinson's disease, although a significant correlation was found in the normal subjects. There was a significant correlation between the P3b latency and Hasegawa's dementia scale (HDS) score although the P3a latency showed no correlation with HDS score. These results indicate that the P3a and P3b components have some differences. In demented patients with Parkinson's disease, the P3b latency was significantly longer than that in 15 age-matched normal subjects, although no significant difference was found in the P3a latency. On the other hand, patients with Alzheimer's disease showed a significant prolongation of both P3a and P3b latencies compared to the age-matched normal subjects. Furthermore, there was a significant difference in P3a latency between demented patients with Parkinson's disease and those with Alzheimer's disease. There were no significant differences in any of the amplitudes among these three groups. These results suggest that the automatic processing stage, as reflected by P3a, may be less impaired than attentional controlled processing reflected by P3b in patients with Parkinson's disease, and further indicate that there may be some differences in the changes of the cognitive process between patients with Parkinson's disease and those with Alzheimer's disease.
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PMID:[Cognitive processes in Parkinson's disease--an event-related potential analysis]. 179 43

We have examined the correlation of dementia severity and brainstem auditory evoked potentials. The subjects were 80 patients with dementia (20 males, 60 females) whose mean age was 80.7 years. Normal controls were 9 elderly subjects (2 males, 7 females) whose mean age was 80.4 years. The following parameters were measured: peak latencies (I, III and V), interpeak latencies (I-III, III-V and I-V) and interaural latency differences (V PLDs and I-V IPLDs). As for clinical items and sex differences; (1) There were sex differences recognized between peak latency of III and V, interpeak latency of III-V and I-V. (2) There was a significant difference in interaural differences of V PL Ds between vascular dementia and degenerative dementia (dementia of the Alzheimer's type and Parkinson's disease). Duration of illness had no correlation with latencies of BAEPs. Dividing the patients into three groups according to the severity of dementia which are mild, moderate and severe, (3) peak latency of III, V and interpeak latency of I-III, III-V, I-V and interaural latency differences of V PL Ds prolonged significantly with the increasing severity of dementia. From these results, it is suggested that brainstem dysfunction progresses with the increasing severity of the dementia.
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PMID:[The severity of dementia and brainstem auditory evoked potentials--peak latency and interpeak latency]. 179 96

Two patients with levodopa-responsive Parkinson's syndrome had numerous cortical and striatal senile plaques and some neurofibrillary tangles at necropsy. In addition neurons in the pars compacta of the substantia nigra were severely depleted but there were no Lewy bodies or other neuropathological changes to account for parkinsonism. Neither patient was demented. These pathological findings have not previously been described as a cause of Parkinson's syndrome without associated dementia of Alzheimer's disease type.
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PMID:Neuropathological features of Alzheimer's disease in non-demented parkinsonian patients. 180 Jun 69

We investigated event-related potentials (P300) in three types of demented patients. Fourteen patients with senile dementia of Alzheimer's type (SDAT), 15 with multiinfarct dementia (MID), 8 with Parkinson's disease with dementia and 29 normal controls participated in this study. We measured the latencies of N100 and P300 at Pz after odd-ball paradigm stimulation. N100 peaks were within the normal range in all patients. However, P300 peaks were significantly delayed in all demented patients. There were no statistical differences in the mean latencies of P300 in each demented group. P300 latencies were found to be negatively correlated with Hasegawa's dementia scale. These results suggest that regardless of its cause dementia has similar influences on the P300 latency and P300 may be a useful means to assess the degree of dementia.
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PMID:Event-related potentials in senile dementia of Alzheimer's type, multiinfarct dementia and Parkinson's disease. 180 Aug 14

Neuronal loss in the substantia nigra (SN) in Parkinson's disease (PD) shows a topographical organisation where the lateral part of the SN is more affected. This is--due to projection of the lateral SN mainly to the putamen--reflected in more complete loss of dopamine content in the putamen than in the caudate nucleus. Of the parkinsonian symptoms rigidity and hypokinesia are associated with neuronal loss in the lateral substantia nigra and the resulting dopamine loss in the putamen. Neuronal mechanisms other than degeneration of the nigrostriatal system seem to be involved in the pathophysiology of tremor. Cognitive impairment and dementia in PD is related to dysfunction of the cortical cholinergic system, especially in the frontal cortex. The brain dopaminergic system, however, contributes as a subcortical component to cognitive impairment in PD. Clinical studies have shown that selegiline may slow down the progression of PD. We studied postmortem samples of patients treated with selegiline and levodopa and those with levodopa alone. The number of medial nigral neurons was significantly higher in the selegiline group. Treatment with selegiline might retard the death of nigral neurons, but further studies are needed to confirm the preliminary findings.
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PMID:Nigral degeneration in Parkinson's disease in relation to clinical features. 180 43


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