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)

We conducted an epitope analysis of senile plaque (SP) proteins on hippocampal SPs in patients with Parkinson's disease (PD), using a library of antibodies to proteins implicated in the genesis of hippocampal SPs in Alzheimer's disease (AD). The library included antibodies to the beta-amyloid protein (beta-AP), domains outside the beta-AP in beta-amyloid precursor proteins (beta-APPs), ubiquitin, diverse neuronal cytoskeletal proteins, and polypeptides located mainly in axon terminals. We obtained samples of hippocampus at autopsy from 14 PD patients, 10 of whom were demented. As in the AD hippocampus, the SPs detected by conventional stains in five of the 10 demented subjects contained the beta-AP and flanking domains in beta-APPs as well as epitopes in tau, neurofilament proteins, and synaptophysin. Further, with the exception of the beta-AP, epitopes in the other proteins were confined to the coronas of SPs, while clathrin light chain, microtubule-associated protein 5, and neural cell adhesion molecules were almost undetectable or absent in the neuropil occupied by SPs. The same group of antibodies rarely labeled SPs in the other five demented PD subjects or in the four nondemented PD subjects, and conventional stains for amyloid and neurofibrillary pathology revealed rare SPs in these cases. Hence, when conventional stains reveal lesions diagnostic of AD in PD patients, the molecular features of the hippocampal SPs in these patients are the same as those in SPs of the AD hippocampus.
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PMID:Epitope analysis of senile plaque components in the hippocampus of patients with Parkinson's disease. 137 4

A Lewy body dementing syndrome in the elderly has been recently described and designated senile dementia of Lewy body type (SDLT) on the basis of a distinct clinicopathological profile. The pathological changes seen in SDLT include the presence of cortical Lewy bodies (LB) frequently, but not invariably, associated with senile plaque (SP) formation. Whilst neocortical neurofibrillary tangles (NFT) are sparse or absent, a proportion of these cases show involvement of the temporal archicortex by lesions comprising Alzheimer-type pathology (ATP, i.e. NFT, SP and granulovacuolar degeneration [GVD]). Thus the relationship between SDLT and senile dementia of Alzheimer type (SDAT) is complex and controversial. In this study quantitative neuropathology was used to compare the intensity and distribution of ATP in the hippocampus and entorhinal cortex of 53 patients from 3 disease groups (SDLT, SDAT, Parkinson's disease (PD)) and a group of neurologically and mentally normal elderly control patients. For most brain areas examined the extent of ATP between the patient groups followed the trend SDAT greater than SDLT greater than PD greater than control. Statistical comparison of these groups revealed significant differences between the mean densities of NFT, SP and GVD although individual cases showed considerable variability. These results confirm additional pathological differences between SDAT and SDLT regarding the intensity of involvement of the temporal archicortex by ATP. Many patients with Lewy body disorders (LBdis) show a predisposition to develop ATP albeit in a more restricted distribution (e.g. low or absent neocortical NFT) and at lower densities than is found in SDAT. Some cases of SDLT show minimal SP and NFT formation in both neocortex and archicortex supporting previously published data distinguishing this group from Alzheimer's disease.
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PMID:Quantitative neuropathological study of Alzheimer-type pathology in the hippocampus: comparison of senile dementia of Alzheimer type, senile dementia of Lewy body type, Parkinson's disease and non-demented elderly control patients. 180 62

Paired helical filaments (PHF), which constitute neurofibrillary tangles (NFT) and neuritic plaque (NP) neurites, serve as a useful marker for Alzheimer disease (AD). We have isolated AD PHF in a highly purified and disaggregated form for use as an immunogen to produce a heterologous polyclonal antiserum in rabbits. One rabbit was maintained long-term for the high quality of the antiserum it produced. Through absorptions with normal brain tissue, we were able to produce a monospecific antiserum which reacts only with NFT and NP neurites in AD brain tissue sections. We further demonstrated the specificity of this antiserum by electron microscopic immunohistochemistry, gel diffusion analysis, and immunoblotting. This antiserum also showed immunoreactivity to NFT of Down syndrome and progressive supranuclear palsy, and to the Pick bodies of Pick disease, but not to the Lewy bodies of idiopathic Parkinson disease. This well-characterized antiserum, all from one rabbit, offers several unique advantages to the study of the nature, origin, and interrelationships of filamentous protein abnormalities in AD and other neurodegenerative disorders.
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PMID:Production and characterization of a monospecific antiserum (A128) to disaggregated Alzheimer paired helical filaments. 211 Feb 8

Deposition of amyloid (A4) protein was assessed in the cerebral cortex of 26 patients dying with various neurodegenerative disorders, other than Alzheimer's disease. Amyloid deposits were (variably) present in 2/3 (66%) elderly (i.e. over 65 years of age) patients with progressive supranuclear palsy, 4/7 (57%) with Parkinson's disease, 2/5 (40%) with Huntington's chorea and in both elderly patients with frontal lobe dementia but were only rarely seen in any patient before this age. The A4 protein deposits were nearly always of a diffuse type with only an occasional 'cored' neuritic plaque being present. Amyloid deposition in elderly persons may thus relate more to certain aspects of ageing and genetics than to AD, per se. Only in this latter condition are the cerebral cortical amyloid deposits widely associated with a neuritic change and a neurofibrillary degeneration of nerve cells.
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PMID:Deposition of amyloid (A4) protein within the brains of persons with dementing disorders other than Alzheimer's disease and Down's syndrome. 213 61

Degenerative diseases of the nervous system which are considered to be related to free radicals are Parkinson's disease and Alzheimer-type dementia (ATD). Parkinson's disease is characterized by appearance of Leyw's body and degeneration of nigrostriatal dopaminergic system. But the most fundamental cause of this disease remains still unknown. The fact that H2O2 is formed in the process of oxidative deamination of catecholamines and some substances which can cause Parkinsonism in animal experiments also produce active oxygen in the metabolic processes suggest the important role of free radicals in the pathogenesis of Parkinson's disease. We recently observed that addition of DOPA and Fe3(+)-ADP complex to the microsomal phospholipid system produced lipid peroxides without participation of active oxygen. Neurons cultured in vitro also decreased significantly with addition of DOPA and Fe3(+)-ADP complex and this harmful effect was prevented by desferoxamine (potent Fe chelating agent) or alpha-tocopherol (antioxidant). These results may suggest that lipid peroxidation can occur by interaction of naturally existing substances in the dopaminergic system and induce cell damage. As regards ATD, there is still no definite evidence to support the implication of free radicals in its pathogenesis. However, there are reports that lipid peroxides increase significantly in the brains of patients with ATD. Moreover, recent advances in the study of amyloid in the senile plaque revealed close relationship of ATD to chromosome 21.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Free radicals and degenerative diseases of the nervous system]. 220 Sep 16

Sensitive silver methods for extracellular amyloid and intraneuronal cytoskeleton abnormalities (neurofibrillary tangles and neuropil threads) were employed to examine the cortical pathology in Parkinson's disease. In cases with cognitive impairment many plaque-like amyloid deposits were found in the cerebral cortex. Neuritic plaques were rare or absent. Neither the Ammon's horn nor the isocortex revealed a sufficiently large number of tangles to permit the diagnosis of a coexisting fully developed Alzheimer's disease. Large numbers of neurofibrillary tangles and neuropil threads were only found in layer Pre-alpha of the entorhinal cortex. This layer gives rise to major portions of the perforant tract, a pathway which serves as a link in the transmission of data from isocortical association areas to the hippocampal formation. During the course of Parkinson's disease the hippocampal formation is thus endangered to become disrupted from isocortical influences. It is concluded that the cognitive impairment shown by many individuals suffering from Parkinson's disease may partly be caused by cortical lesions.
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PMID:Cognitive impairment in Parkinson's disease: amyloid plaques, neurofibrillary tangles, and neuropil threads in the cerebral cortex. 235 70

A 68 year old male, diagnosed as Alzheimer's disease clinically, pathologically showed both findings of Alzheimer's disease and Parkinson's disease. The brain weight was 940 g. Macroscopically, severe cortical brain atrophy and depigmentation of the substantia nigra was noted. Microscopic examination showed marked appearance of senile plaque and a large number of neurofibrillary tangle with sever neuronal loss of the cerebral cortex. Additionally, the loss of neuron with many Lewy bodies was found in the substantia nigra. Lewy bodies were also found in the locus ceruleus and the dorsal vagal nucleus, but few in the cerebral cortical neurons. We compared this case neuropathologically with two autopsy cases of diffuse Lewy body disease (DLBD). There was no distinction concerning the lesions of the brain stem between this case and the cases of DLBD. In all three cases, the nucleus of basalis of Meynert showed marked neuronal loss. However, the brain was lighter than those of the cases of DLBD. Senile changes such as senile plaque and neurofibrillary tangles were more marked in this cases than in the cases of DLBD. Furthermore a large number of cortical Lewy bodies were found in the cases of DLBD, but few in this case. The distribution and number of Lewy bodies did not correspond with those of senile changes in the cases of DLBD. Also the cerebral cortical structure was better preserved in the cases of DLBD than in this case. In conclusion, from the clinicopathological findings, we considered that this case is Alzheimer's disease associated with Parkinson's disease. According to Kosaka's study, this case seemed to correspond with a transitional type of the Lewy body disease.
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PMID:[An autopsy case of Alzheimer's disease associated with Parkinson's disease, compared to 2 autopsy cases of diffuse Lewy body disease]. 238 95

The pedunculopontine and laterodorsal tegmental nuclei comprising the pontomesencephalotegmental (PMT) cholinergic system were examined for the presence of neuropathology and loss of presumed cholinergic cells in patients diagnosed with Alzheimer's disease-senile dementia of the Alzheimer type (AD-SDAT), Parkinsonian dementia, and multi-infarct dementia. Although neurofibrillary changes and plaque-like entities were observed in both nuclei in AD-SDAT and Parkinson's disease dementia, these pathologic indices were not seen consistently in control individuals or in those with multi-infarct dementia, and in none of the diagnostic categories was loss of neuronal somata found in the PMT cholinergic complex. Because appreciable degeneration of cholinergic neurons does occur in the basal forebrain in AD-SDAT, it is concluded that cholinergic phenotype alone is not a sufficient condition indicating predilection for neuronal loss in that dementing illness.
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PMID:The pontomesencephalotegmental cholinergic system does not degenerate in Alzheimer's disease. 271 53

The evidence for deficiencies in neurotransmitters in Alzheimer's disease is reviewed. Major losses occur in the subcortical afferent projection systems based on acetylcholine, noradrenaline and serotonin. Within the cortex, somatostatin containing neurones and the large pyramidal cells, presumed to use glutamate/aspartate as transmitters, are the most severely damaged cells. The anatomical distribution of cell loss is explainable if the primary site of damage lies within the cortex; nerve cells are damaged by virtue of their presence within or their connections to this region. The senile plaque may represent the site of this damage and neurofibrillary tangle formation and accumulation may lead to cell death. In patients with Down's syndrome who live past 40 years, changes in transmitters apparently identical to those in Alzheimer's disease occur. The dementia of Parkinson's disease appears related to damage to cholinergic, noradrenergic and dopaminergic systems and may reflect a failure of these subcortical regions to sufficiently "activate" an otherwise undamaged cortex.
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PMID:Neurotransmitter deficits in Alzheimer's disease and in other dementing disorders. 287 73

Neurofibrillary tangles occur in a number of apparently distinct neurodegenerative diseases and in normal aging of the human brain. Antibodies raised against Alzheimer's disease paired helical filaments immunolabel the tangles seen in all other tangle-associated disorders examined to date. The neuronal microtubule-associated protein, tau, has recently been identified as an antigenic component of neurofibrillary tangles and senile plaque neurites in Alzheimer's disease. Three different polyclonal antibodies with strong tau immunoreactivity are examined in this study. These antibodies were found to immunostain tangles in normal aged brain and in brains affected by a range of neurodegenerative disorders, including Down's syndrome, Alzheimer's disease plus Parkinson's disease, progressive supranuclear palsy, and the parkinsonism-dementia complex of Guam, as well as Pick bodies in Pick's disease. The findings further illustrate the relative nonspecificity of neurofibrillary lesions in neurodegenerative disorders.
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PMID:Tau antisera recognize neurofibrillary tangles in a range of neurodegenerative disorders. 296 85


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