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)

Antibodies reacting with neuronal cytoplasmic antigens present in normal human caudate and subthalamic nuclei were detected in 37 of 80 probands afflicted with Huntington's disease (HD). IgG antibodies were detected by immunofluorescence using frozen sections of unfixed normal human and rat brain. Specificity of IgG binding was confirmed using pepsin F(ab')2 fragments of IgG isolated from positive sera. In vitro complement fixation of IgG antibody was detected in 22 of 31 sera tested. Neuronal cytoplasmic antigens reacting with positive HD sera were diminished after trypsin or RNAase treatment of tissue sections but were not removed by DNAase, neuraminidase, EDTA, or dithiothreitol treatment. Antibody staining of neurons could be removed after absorption with isolated caudate nucleus neurons or by using perchloroacetic acid extracts of caudate nucleus. Prevalence of antibody reacting with neuronal cytoplasm was 3% in 60 normal controls and 6% among a wide variety of patients with diverse neurological disorders. However, one-third of 33 patients with Parkinson's disease showed presence of antineuronal antibody. Among patients with HD, a significant association was noted between duration of clinical disease greater than 7 yr and titers of antibody of 1:2 or greater (P less than 0.001). When 115 family members of HD probands were tested, 30% of unaffected spouses showed presence of antineuronal antibody. 23.2% of first-degree relatives at risk for developing HD was also positive (P less than 0.001). 10.5% of second-degree relatives showed presence of antineuronal antibody. These data may support an environmental or infectious factor somehow involved in the ultimate expression of HD.
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PMID:Antibodies to human caudate nucleus neurons in Huntington's chorea. 14 Jan 83

The lateral tuberal nucleus is a circumscribed cell mass in the lateral posterior part of the hypothalamus, containing about 60000 neurons. It can be recognized in man and higher primates, probably not in other mammals. Its neurotransmitter content and connections with other parts of the brain are as yet unknown. But receptors for corticotropin-releasing factor and somatostatin, as well as muscarinic cholinergic receptors, benzodiazepine receptors and N-methyl-D-aspartate receptors have been localized within the confines of the nucleus. The lateral tuberal nucleus is affected in a number of human neurodegenerative diseases. Changes in Parkinson's disease are the least obvious: Lewy bodies appear in small amounts, the majority of them apparently lying outside a neuronal perikaryon. Neuronal loss does not occur. In Alzheimer's disease the number of neurons seems to be normal as well. Rarely silver staining tangles occur, and the deposition of A4/beta-protein in amorphous plaques is moderate. Yet, NTL neurons stain heavily in Alz-50 immunocytochemistry, while Alz-50 staining in NTL neurites is very dense. These changes are interpreted as indicating early Alzheimer-related pathology. In Huntington's disease the NTL loses neurons. This loss is related to the severity of the disease: patients who first display motor disturbances at an early age will lose more neurons than those who start later. The relation between these clinical characteristics and the severity of neuronal loss is such, that it seems likely that NTL neurons possess a special vulnerability for the effect of the Huntington gene. This could be related to their NMDA-receptor content. It is hypothesized that the NTL is involved in a neuronal network that regulates feeding and metabolism. NTL pathology may explain the peculiar catabolic state of many patients with Alzheimer's or Huntington's diseases.
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PMID:The hypothalamic lateral tuberal nucleus: normal anatomy and changes in neurological diseases. 136 79

Neuronal thread protein is a recently characterized, approximately 20-kd protein that accumulates in brains with Alzheimer's disease (AD) lesions. This study examined whether concentrations of neuronal thread protein (NTP) were also increased in the cerebrospinal fluid (CSF) of individuals with probable (clinically diagnosed) and definite (histopathologically proved) AD. Using a highly sensitive three-site monoclonal antibody-based immunoradiometric assay, we measured NTP concentrations in CSF from 84 patients with probable AD and mild dementia (duration, 4.05 +/- 0.36 years), 45 with Parkinson's disease and minimal or no dementia (duration, 4.73 +/- 0.78 years), 73 with multiple sclerosis, and 73 nondemented control subjects. NTP concentrations were also measured in postmortem ventricular fluid and temporal lobe neocortex extracts from 31 subjects with histopathologically proved AD and 14 age-matched control subjects. The mean concentration of NTP in the CSF was higher in AD (4.15 +/- 0.25 ng/ml; 95% confidence interval [CI] limits, 3.65-4.65) than in Parkinson's disease (1.96 +/- 0.16 ng/ml; 95% CI, 1.65-2.27), multiple sclerosis (1.6 +/- 0.14 ng/ml; 95% CI limits, 1.33-1.88), or control subjects (1.27 +/- 0.06 ng/ml; 95% CI limits, 1.15-1.40) (p < 0.001). In addition, 70% of the patients with probable AD had concentrations of NTP in CSF that were higher than 2.5 ng/ml (> upper 99% CI limit in the control group), compared with 23% of Parkinson's disease patients, 11% of multiple sclerosis patients, and 4% of control subjects. The mean concentrations of NTP in the ventricular fluid and brain tissue from individuals with documented AD and end-stage dementia were threefold higher than the levels detected in the CSF from the remaining patients with probable AD and mild dementia. Moreover, of 9 patients with AD, postmortem brain and CSF manifested 5- to 50-fold higher levels of NTP compared with the CSF samples obtained an average of 6 years earlier. These findings demonstrate that NTP levels are elevated in the CSF of individuals with AD and that NTP levels in the CSF increase strikingly with progression of dementia and neuronal degeneration.
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PMID:Increased levels of neuronal thread protein in cerebrospinal fluid of patients with Alzheimer's disease. 147 63

Neuronal thread protein (NTP) is a recently characterized molecule that is over-expressed in brains with Alzheimer's disease (AD) lesions. The present study encompasses a detailed analysis of NTP expression in AD compared with other neurodegenerative diseases and aged controls. Using a specific monoclonal antibody, NTP immunoreactivity was evaluated in 309 paraffin-embedded sections from 8 different regions of the frontal, parietal, and temporal lobes of 73 brains with AD, AD + Down's syndrome (DN), AD + Parkinson's disease (PD), PD dementia (PDD), aged controls, and disease controls with Huntington's disease, multi-infarct dementia, or schizophrenia. In 250 adjacent blocks of snap-frozen unfixed tissue the concentration of NTP (ng/mg of protein) was measured using a 3-site forward sandwich monoclonal antibody based immunoradiometric assay (M-IRMA). Immunohistochemical studies demonstrated that brains with AD, AD + PD, and AD + DN contained significantly higher densities of NTP immunoreactive neurons and more frequent immunostaining of neuropil and white matter fibers compared with PDD and aged controls (both P < 0.001) which had few or no AD lesions. In addition, the overall mean concentrations of NTP in AD, AD + PD, and AD + DN were significantly higher than in PDD and aged controls (P < 0.005). Greater degrees of NTP immunoreactivity and higher concentrations of the protein in cerebral tissue were significantly correlated with AD diagnosis and abundant neurofibrillary tangles (P < 0.005). The findings suggest that NTP over-expression may serve as a marker for the type of neuronal degeneration that occurs in AD.
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PMID:Neuronal thread protein over-expression in brains with Alzheimer's disease lesions. 148 53

Clinical and neuropathologic data in 45 patients with Parkinson's disease (PD) were compared. Twenty-seven patients suffered from marked akinesia and rigidity (AR-type) and 18 patients from predominant resting tremor (T-type). Dementia, depression, and psychosis occurred in 26, 18, and 18 patients, respectively. Neuronal counts were performed in defined areas of the medial and lateral substantia nigra (SNM, SNL), locus ceruleus (LC), and dorsal raphe nucleus (DRN). The AR-type (compared with the T-type) showed higher neuronal loss of LC, SNL, SNM, and more severe gliosis, extraneuronal melanin deposits, and neuroaxonal dystrophy in substantia nigra. Demented PD patients showed more intense cortical Alzheimer lesions and higher neuronal depletion in the SNM, whereas PD subjects with moderate or marked dementia differed from mildly or not demented ones only in the higher degree of cortical Alzheimer lesions. More severe neuronal cell loss of DRN was observed in PD patients with depression. Occurrence of psychosis was not associated with any pathologic feature. Our findings indicate that some major clinical features of PD are related to distinct neuropathologic lesions.
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PMID:The neuropathologic basis of different clinical subgroups of Parkinson's disease. 174 81

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

Neuronal subpopulations of the substantia nigra pars compacta can be separated into two functionally distinct nigrostriatal projections, the ventral tier which is poorly melanised, and the dorsal tier which is well melanised. In Parkinson's disease, juvenile-onset parkinsonism with dystonia and striatonigral degeneration the ventral tier is more vulnerable than the dorsal tier. The ventral tier mostly projects to the putamen, which is vulnerable in striatonigral degeneration and Huntington's disease. In Huntington's disease spiny neurons of the striatal matrix and neurons of the pars reticulata are particularly susceptible. Determining patterns of selective neuronal death may lead to identification of pathogenetic mechanisms.
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PMID:Neuropathology of the substantia nigra. 183 Feb 74

Three patients with clinical and pathological features of corticobasal degeneration are described. They presented with a progressive disease bearing some clinical resemblance to Steele-Richardson-Olszewski syndrome and displaying some pathological features of Pick's disease. Their illness began at the age of 59 to 66 yrs with focal dystonia and myoclonus of an arm, the 'alien hand' sign, or an akinetic-rigid syndrome. They developed a supranuclear gaze palsy, parkinsonian features and mild cerebellar signs. Two patients showed constructional dyspraxia when using the arms. The duration of disease to death was 4 to 6 yrs. Pathological examination showed frontoparietal atrophy with cortical cell loss, gliosis and Pick cells, but there was no significant hippocampal disease or Pick bodies in this region. There was nerve cell loss and gliosis in the thalamus, lentiform nucleus, subthalamic nucleus, red nucleus, midbrain tegmentum, substantia nigra and locus coeruleus. Neuronal inclusions in the substantia nigra, termed corticobasal inclusions, were reminiscent of the globose neurofibrillary tangle of Steele-Richardson-Olszewski syndrome, and other pale inclusions resembled the pale body of Parkinson's disease, but Lewy bodies and neurofibrillary tangles were generally absent. Some nigral inclusions were similar to those in Pick's disease. Despite some pathological similarities to Pick's disease we suggest that the distribution of nerve cell loss and the corticobasal inclusion are unique to corticobasal degeneration.
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PMID:Corticobasal degeneration. 2059 45

Alterations of the coeruleo-cortical adrenergic system in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced monkey parkinsonism were examined through neuropathological observation and radioreceptor assay. Neuronal degeneration was found not only in the substantia nigra but also in the locus coeruleus of all the MPTP-treated monkeys. From radioreceptor assay, decreases of alpha 1 and alpha 2 receptors in the parietal and temporal cortices were observed in parkinsonian monkeys. In addition, beta receptors increased in the temporal cortex. These changes in monkey parkinsonism are very similar to those in human Parkinson's disease.
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PMID:Alterations of the central noradrenergic system in MPTP-induced monkey parkinsonism. 284 89

The rostal mesencephalon at the level of the posterior commissure was studied by light microscopy in two patients with idiopathic Parkinson's disease, one patient with Alzheimer's disease, and one patient with senile dementia of Alzheimer's type. In the Parkinsonian cases, the rostral part of the nucleus of Edinger Westphal disclosed Lewy bodies in 3% of the neurons, neurofibrillary degeneration in 2% of the neurons, and a 54% neuronal loss. In Alzheimer's disease, 2% of Edinger Westphal neurons contained neurofibrillary degeneration, whereas in senile dementia of Alzheimer's type only rare neurofibrillary degeneration was evident in this nucleus. Neuronal loss was not apparent in the nucleus of Edinger Westphal in either of the Alzheimer's cases. The pathologic changes observed in this presumably cholinergic nucleus resemble in some respects changes reported in the cholinergic centers of the basal forebrain in these diseases. In addition, the central gray matter and pretectal region in Parkinson's disease contained a patchy increase in astroglia, some with scant reactive cell bodies; however, Lewy bodies were limited to that part of the central gray matter corresponding to the nucleus of Darkschewitsch. A few neurofibrillary tangles were present in the nucleus of Darkschewitsch in both diseases.
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PMID:The rostral mesencephalon in Parkinson's disease and Alzheimer's disease. 299 84


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