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)

A4 protein (beta-protein, beta-amyloid) deposits were identified with silver stains in postmortem brainstem sections from 13 patients with Alzheimer disease (AD), 6 patients with mixed Alzheimer disease and Parkinson disease (AD-PD), 5 disease controls, and 2 elderly controls. A rostro-caudal gradient of A4 was found in patients with AD and AD-PD, such that A4 was most prevalent in the midbrain and least prevalent in the medulla. The brainstem of the controls contained little or no A4. The midbrain tectum and tegmentum contained the greatest densities of A4, but the red nucleus and substantia nigra pars reticulata were largely spared. This distribution of A4 suggests that A4 deposition is a function of synaptic connectivity rather than passive diffusion from vascular sources.
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PMID:Distribution of amyloid in the brainstem of patients with Alzheimer disease. 130 Apr 98

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

Silver techniques for intraneuronal cytoskeleton abnormalities (neurofibrillary tangles and neuropil threads) and extracellular A4-amyloid deposits were used to examine lesions of the cerebral cortex in six cases of progressive supranuclear palsy (three were mentally unimpaired and three showed moderate degrees of dementia). Deposits of A4-amyloid protein occurred in small numbers or were absent. Neurofibrillary tangles and neuropil threads were present in all cases and were largely confined to the allocortex. A characteristic pattern of changes was found in the entorhinal cortex. The three mentally unimpaired individuals had mild cortical changes virtually confined to the transentorhinal region while all of the demented patients showed severe destruction of the superficial cellular layer in both the transentorhinal and entorhinal region. This pattern of allocortical destruction closely resembles that seen in clinically incipient Alzheimer's disease or in mentally impaired cases of Parkinson's disease. The entorhinal region receives dense input from isocortical association areas and projects via the perforant path to the hippocampal formation. The cells of origin of major portions of the perforant path are located within the superficial entorhinal cellular layer. Destruction of this layer partially or totally disconnects the hippocampus from the isocortex. The specific pattern of entorhinal destruction is considered to contribute to cognitive impairment and personality changes, frequently seen in patients with progressive supranuclear palsy.
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PMID:Allocortical neurofibrillary changes in progressive supranuclear palsy. 146 62

Foamy spheroid bodies (FSBs) are described, as newly identified pathological structures occurring in human brain. FSBs favoured the substantia nigra pars reticulata (SNPR) and/or globus pallidus (GP) in degenerative conditions especially postencephalitic parkinsonism, progressive supranuclear palsy, pallido-nigro-luysial atrophy and multiple system atrophy. No FSBs were observed anywhere in the presence of substantia nigra pars compacta (SNPC) degeneration, such as occurs in idiopathic Parkinson's disease, or luysio-pallidal system degeneration, such as found in dentato-rubro-pallido-luysial atrophy or Joseph's disease. FSBs were also occasionally identified in the substantia nigra (SN) and/or GP of aged persons. In addition to SN and GP lesions, FSBs were seen in diffuse axonal lesions of long fibre tracts (the corpus callosum, the superior cerebellar peduncle) after non-missile head injuries, and in peri-infarct lesions. Under the light microscope, FSBs appear as slightly eosinophilic, foamy and nearly round objects with vague outlines, measuring approximately 10-50 microns in diameter. Some FSBs contain coarse, eosinophilic clusters at their periphery. FSB stained black when stained by the Gallyas silver method. Some FSBs were immunohistochemically positive for synaptophysin and 68 kDa neurofilament. Glial fibrillary acidic protein-positive fibres were observed alongside and/or inside some FSBs. Electron microscopically, FSBs were found to consist of collections of neuritic debris containing a variety of dense bodies and a small number of both mitochondria and neurofilaments. Some such collections were surrounded by astrocytic processes. These findings strongly suggest that FSBs are collections of small axonal debris destined for removal by astrocytes in due course. A variety of factors (degeneration of the SNPR and/or the GP, injury, infarction, ageing) seemed to be responsible for the histogenesis of FSBs.
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PMID:Peculiar axonal debris with subsequent astrocytic response (foamy spheroid body). A topographic, light microscopic, immunohistochemical and electron microscopic study. 155 16

The parabrachial nucleus is believed to play a role in autonomic regulation. We have used the Fontana-Masson ammoniacal silver nitrate method and a tyrosine hydroxylase-immunostaining technique to demonstrate the presence of neuromelanin-containing catecholaminergic neurons in the parabrachial nucleus of normal individuals. In addition, we also show that there is a significant reduction of these catecholaminergic neurons and presence of Lewy bodies in the parabrachial nucleus of patients with idiopathic Parkinson's disease. These findings may be related to the several autonomic disturbances that may occur in idiopathic Parkinson's disease.
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PMID:Catecholaminergic neurons in the parabrachial nucleus of normal individuals and patients with idiopathic Parkinson's disease. 168 Mar 3

In the present study, quantitative in situ hybridization was used to analyse the effect of haloperidol treatment on D2 dopamine receptor gene expression in the rat caudate-putamen nucleus. Variations of D2 receptor mRNA level were studied and measured at the macroscopic level of densitometric analysis of X-ray film and at the microscopic level by counting of autoradiographic silver grains in striatal cells. Macroscopic analysis demonstrated that haloperidol treatment two times 1 mg/kg per day during seven, 14 and 21 days increased D2 receptor mRNA level in the caudate-putamen. Detailed microscopic analysis demonstrated a significant increase in D2 receptor mRNA in the two neuronal populations known to express the D2 receptor gene: medium-sized neurons previously identified as enkephalinergic neurons, and large-sized neurons previously identified as cholinergic neurons. The increase was more important in cholinergic neurons (+119%) than in enkephalinergic neurons (+54%). Haloperidol treatment did not modify the number of medium-sized enkephalinergic neurons expressing the D2 receptor mRNA. In contrast, it significantly increased the percentage of large-sized neurons containing D2 receptor mRNA (from 80 to 94%). These results demonstrate that haloperidol treatment acts at the gene level to modulate D2 receptor content in striatal dopaminoceptive neurons, and that the D2 receptor mRNA increase in postsynaptic neurons contributes to dopamine supersensitivity induced by neuroleptics in the rat. This suggests that dopamine acts trans-synaptically to control D2 receptor gene expression in target striatal neurons. These results suggest that modifications of D2 receptor gene expression may be part of the biological events that lead to the movement disorders induced by neuroleptic drugs or Parkinson's disease.
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PMID:Striatal neurons express increased level of dopamine D2 receptor mRNA in response to haloperidol treatment: a quantitative in situ hybridization study. 175 61

Two distinct neuronal inclusions occur in Parkinson's disease. The Lewy body is the diagnostic hallmark and is recognized by its eosinophilic body and unstained halo. It can be found in specific regions of the nervous system, where its frequency, size, shape, and structure differ. Large neurons of the dorsal vagal nucleus and sympathetic ganglia often contain particularly large quantities of Lewy-body-like matter. It consists of filament in the outer part and electron dense material in the core, the outer part staining with silver and with antibodies to neurofilament and tubulin. The pale body is restricted to the substantia nigra and locus ceruleus. It does not react with conventional stains, silver, or neurofilament antibodies, and has a homogeneous structure with a granular and vesicular surface texture. It contains sparse granular matter, vacuoles, and filaments, surrounded by melanin. The Lewy body and pale body may be juxtaposed or contiguous in some cells, but their distinct appearances and structures indicate that they are separate inclusions.
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PMID:Neuronal inclusions of Parkinson's disease. 184 77

The contents of indispensable major elements sodium (Na), phosphorus (P), calcium (Ca), magnesium (Mg), trace elements iron (Fe), copper (Cu), nickel (Ni), zinc (Zn), strontium (Sr), vanadium (V), chromium (Cr), manganese (Mn), molybdenum (Mo), and other elements lead (Pb), silicon (Si), aluminium (Al), titanium (Ti), barium (Ba), lanthanum (La), cadmium (Yb), cerium (Ce), scandium (Sc), silver (Ag), in cerebrospinal fluid (CSF) were measured in 13 patients suffering from Parkinson disease before and after autotransplantation of adrenal medulla. It was found that while the patients' objective symptoms were relieved and the contents of monoamine transmitters were changed, the contents of P, V, Co, Cr, in CSF increased significantly (P less than 0.05 or 0.01) at the first, 2nd, 4th, 6th, and 8th week, the contents of Mn in CSF also increased significantly at the first 4th week (P less than 0.05) but decreased significantly at the 8th week the contents of Zn in CSF increased significantly (P less than 0.05) at the 2nd week; Mo increased significantly (P less than 0.05 or 0.01) at the 4th and 8th week B increased significantly (P less than 0.05) at the first week; the contents of Ca, Na, Sr, Ba, Al, Ti, La, Ce, Yb, Sc, Ag in CSF increased significantly (P less than 0.05 or 0.01) at the 8th week, Mg, Fe, Cu Ni, Pb, Si, Cd remained unchanged after operation. The results suggest that the contents of these chemical elements can be affected by this kind of operation, indicating that these elements are involved in the pathogenesis of Parkinsonism.
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PMID:[Determination of multiple chemical elements in CSF in Parkinson disease after intracerebral autotransplantation of the adrenal medulla]. 186 88

The cerebrospinal fluid (CSF) is a specific ultrafiltrate of plasma, which surrounds the brain and spinal cord. The study of its proteins and their alteration may yield useful information on several neurological diseases. By using various electrophoretic separation techniques, several CSF proteins have been identified derived from plasma or from brain. Different one-dimensional methods, such as agarose gel electrophoresis and isoelectric focusing, are of similar value in identifying the non-specific oligoclonal bands, which are mainly helpful in the diagnosis of multiple sclerosis and other inflammatory diseases. Isoelectric focusing has a greater resolution than other one-dimensional methods, and it yields additional data about disease-associated proteins occurring in Alzheimer's disease, Huntington's chorea and amyotrophic lateral sclerosis. Silver-stained two-dimensional gels provide more information about the complex protein composition of CSF, particularly about proteins produced in the brain, such as apolipoprotein E and neuron-specific enolase. For the detection of oligoclonal antibodies, the investigation of protein changes revealed by Parkinson's disease, schizophrenia and Creutzfeldt-Jakob disease, and the analysis of CSF immune complexes, two-dimensional electrophoresis has a greater sensitivity.
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PMID:Analysis of cerebrospinal fluid proteins by electrophoresis. 193 90

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


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