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)

Expression of chromogranin A in various neurological diseases was examined immunohistochemically using purified anti-human chromogranin A antiserum. The antibody stained dystrophic neurites in senile plaques in Alzheimer disease brain, Pick bodies and ballooned neurons in Pick's disease brain, some Lewy bodies in the substantia nigra of Parkinson's disease, and axonal swellings in various neurological conditions including Parkinson's disease, striatonigral degeneration, Shy-Drager syndrome, amyotrophic lateral sclerosis and cerebral infarction. The present study shows that expression of chromogranin A is not an exclusive feature of Alzheimer disease or Pick's disease, and indicates that it could be a useful marker for various neurological diseases.
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PMID:Expression of chromogranin A in lesions in the central nervous system from patients with neurological diseases. 804 89

We investigated the profile of cognitive and memory deficits of 22 Parkinson's disease (PD), 24 amyotrophic lateral sclerosis (ALS) patients and 26 age-matched controls. The patients were at the early phase of the disease and untreated. The ALS patients exhibited deficits in simple visuoperceptual functions and in complex visuoperceptual reasoning (Digit Symbol and Block Design tests), whereas the PD patients showed deficits only in simple visuoperceptual functions. Moreover, both ALS and PD patients had impairment in tasks requiring set shifting from one reaction to another that may suggest frontal lobe dysfunction. The ALS and PD patients also showed impairment in the task of learning a word list with effort-demanding organization of the material to be remembered. However, preserved delayed recall of logical passages suggests that memory, per se, is not impaired in ALS or in PD. The patterns of errors in a test of recognition of learned words imply, at least partially, different underlying deficits in the two diseases. An inability to inhibit irrelevant information may contribute to memory impairment in ALS patients, whereas the memory deficit in PD may derive from lowered motivation or initiating behaviour.
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PMID:Cognitive and memory deficits in untreated Parkinson's disease and amyotrophic lateral sclerosis patients: a comparative study. 811 9

The expression of heat shock proteins (hsp) within the target organ is implicated in the pathogenesis of a number of diseases of suspected autoimmune etiology, including MS. To pursue the potential role of a humoral response to the hsp 60/65 kd family in MS, we studied serum and CSF by Western blotting using recombinant Mycobacterium bovis hsp 65 and human hsp 60 as antigens and compared the findings with samples from patients with other neurologic diseases (OND). Analysis of the IgG response in CSF from 18 patients with MS indicated moderate reactivity in 10 cases and no reactivity in eight. In the OND group, reactivity was found in the CSF from one of two patients with Parkinson's disease, four of four Alzheimer's disease patients, and two of two patients with amyotrophic lateral sclerosis. CSF samples from seven of seven patients with subacute sclerosing panencephalitis were negative, as were samples from two normal subjects. There was no reactivity in CSF from two Huntington's disease patients. We conclude that antibodies reactive with hsp 60/65 are present in CSF of some MS patients but are also present in a number of chronic neurodegenerative conditions. The findings indicate that a humoral response to hsp 60/65 in the CSF is not specific for MS.
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PMID:Humoral response to hsp 65 in multiple sclerosis and other neurologic conditions. 819 Mar 1

Alz-50 is a monoclonal antibody that recognizes normal tau proteins as well as phosphorylated tau proteins that are associated with paired helical filaments in Alzheimer's disease. To establish an accurate baseline for future pathological studies, we examined the distribution of Alz-50 immunoreactivity in normal human brain from infancy to senescence. We found extensive staining patterns of somata and axonal profiles in the striatum, amygdala, hypothalamus, brainstem and spinal cord in all normals at all ages. Similar normal staining patterns were seen in the brains of patients who had suffered trauma, tumors, cerebral infarcts, grade 1 periventricular hemorrhages, and in those who had suffered from amyotrophic lateral sclerosis, Parkinson's disease, multi-systems atrophy and Shy-Drager syndrome. An absence of cell body staining and only minimal axonal staining was noted in the same brains with immunocytochemistry using PHF-1, a monoclonal antibody generated against paired helical filament proteins from Alzheimer brains. The characteristic staining pattern of Alz-50 in normal brains is substantially more extensive than has previously been recognized. This pattern, which presumably describes a specific class of tau proteins, must be distinguished from the pathological staining observed in neurodegenerative diseases.
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PMID:The distribution of Alz-50 immunoreactivity in the normal human brain. 823 10

Ubiquitinated cytoplasmic inclusions are a characteristic feature of the neuronal pathology of neurodegenerative diseases. Immunocytochemical techniques have identified intermediate filaments associated with ubiquitin-immunoreactive inclusions in Alzheimer's disease (AD), Parkinson's disease (PD), and Pick's disease; however, no core protein has been detected in the ubiquitinated inclusions in amyotrophic lateral sclerosis (ALS). The pathogenesis of these inclusions is not known, but the inclusion may result from an accumulation of an abnormal proteins. Here we report a novel protein of 32.5 kDa detected by polyacrylamide gel electrophoresis, in the spinal cord in ALS patients. A polyclonal antibody raised against this protein and used for Western blotting, suggests that the novel protein is related to actin. Immunocytochemical studies using this antibody indicate that the protein is found in Lewy body-like inclusions in anterior horn cells of ALS, and in Lewy bodies in the substantia nigra in PD.
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PMID:Antibody to an abnormal protein in amyotrophic lateral sclerosis identifies Lewy body-like inclusions in ALS and Lewy bodies in Parkinson's disease. 824 23

This issue focuses on the potential utilization or involvement of growth factors in Alzheimer's disease, amyotrophic lateral sclerosis, Parkinson's disease, and epilepsy. Certainly, the role of growth factors in other neurological disorders associated with stroke, trauma, and neurodegeneration needs to be considered. While there is no direct evidence to indicate that a neurological disorder is associated with the compromised function of a specific growth factor, the use of these molecules as therapeutic agents is justifiable. Undoubtedly, the outcome of current clinical trials will certainly influence future decisions on the use of growth factor therapies.
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PMID:Experimental evidence for growth factor treatment and function in certain neurological disorders. 828 74

Idiopathic parkinsonism (Parkinson's disease) makes up the largest diagnostic subgroup of patients with parkinsonism. Various hypotheses exist regarding the pathogenesis of idiopathic parkinsonism: these include genetic predilection aging, environmental factors, oxidative stress, excitotoxicity, autoimmunity, and trauma. We suggest that the pathogenesis of idiopathic parkinsonism is likely to be multifactorial, deriving from environmental factor(s) acting upon a genetically predisposed individual. Because of the compelling evidence indicating common clinical and pathological findings in idiopathic parkinsonism, Alzheimer's disease, and amyotrophic lateral sclerosis, we believe that these conditions result from pathological processes with more similarity than diversity. A primary glutamatergic cell neocortical abnormality provides an attractive unifying explanation which may explain the overlapping abnormalities found in idiopathic parkinsonism, Alzheimer's disease, and amyotrophic lateral sclerosis.
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PMID:Pathogenesis of idiopathic parkinsonism. 837 34

The Chamorro population of the island of Guam is highly susceptible to a disease called lytico-bodig (LB), which clinically resembles a mixture of amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD) and Alzheimer disease (AD). The disease is characterized by the widespread development of neurofibrillary tangles in the central nervous system. These tangles have an immunohistochemical profile indistinguishable from that seen in AD. We studied by immunohistochemistry the occurrence of intracellular and extracellular neurofibrillary tangles in LB in the entorhinal cortex, hippocampus and substantia nigra using antibodies to tau protein and ubiquitin. We also studied the relationship of these tangles to amyloid precursor protein (APP) and its beta-amyloid fragment (BAP), using multiple antibodies to BAP and other APP sequences. In advanced cases of LB, the development of neurofibrillary tangles was far more severe than in advanced cases of AD. Virtually all neurons of CA-1 and the subiculum were lost and only ghost tangles remained. In areas dominated by such extracellular tangles, BAP deposits were frequently observed developing around the fibers of ghost tangles. In some cases, the deposits covered only a few of the fibers, but in others, they seemed to envelope the complete tangle. The deposits were thioflavin S and Congo red positive, indicating that the BAP was in a consolidated form. We describe these entities as "tangle-associated amyloid deposits". Such BAP deposits have previously been described in some cases of AD, dementia pugilistica and LB. However, we found them in all cases of LB with dementia in the hippocampal-entorhinal areas and in most cases in the substantia nigra. They do not evolve from diffuse BAP deposits since they are remote from them, and they do not trap dystrophic neurites. The fact that extracellular tangle material can act as a nidus for BAP build-up in LB suggests that further consideration needs to be given to the ways in which extracellular BAP deposits are formed.
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PMID:Relationship of amyloid beta/A4 protein to the neurofibrillary tangles in Guamanian parkinsonism-dementia. 852 3

Defects in mitochondrial energy production have been implicated in several neurodegenerative disorders, such as Parkinson disease and amyotrophic lateral sclerosis. To study the contribution of mitochondrial defects to Alzheimer disease and schizophrenia, cytochrome-c oxidase (COX) activity and levels of the mtDNA4977 deletion in postmortem brain tissue specimens of patients were compared with those of asymptomatic age-matched controls. No difference in COX activity was observed between Alzheimer patients and controls in any of five brain regions investigated. In contrast, schizophrenic patients had a 63% reduction of the COX activity in the nucleus caudatus (P < 0.0001) and a 43% reduction in the cortex gyrus frontalis (P < 0.05) as compared to controls. The average levels of the mtDNA4977 deletion did not differ significantly between Alzheimer patients and controls, and the deletion followed similar modes of accumulation with age in the two groups. In contrast, no age-related accumulation of mtDNA deletions was found in schizophrenic patients. The reduction in COX activity in schizophrenic patients did not correlate with changes in the total amount of mtDNA or levels of the mtDNA4977 deletion. The lack of age-related accumulation of the mtDNA4977 deletion and reduction in COX activity suggest that a mitochondrial dysfunction may be involved in the pathogenesis of schizophrenia.
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PMID:Decreased cytochrome-c oxidase activity and lack of age-related accumulation of mitochondrial DNA deletions in the brains of schizophrenics. 853 74

We investigated the number of tyrosine hydroxylase (TH)-immunoreactive neurons in the C1 and A2 regions of the medulla, the sites of the baroreflex arc, in 7 patients with multiple system atrophy (MSA), 8 with Parkinson's disease (PD), 9 with amyotrophic lateral sclerosis (ALS), and 12 age-matched normal subjects to analyze the relationship between cardiovascular dysfunction and medullary catecholaminergic neurons. Orthostatic hypotension (OH) was marked in all the MSA patients and moderate in three PD patients. Three of the five ALS patients who had been on respirators showed lability of blood pressure; paroxysmal hypertension and nocturnal hypotension without compensatory tachycardia. All the MSA patients showed extremely marked decrease of TH-immunoreactive neurons in both the C1 and A2 regions. In the patients with Parkinson's disease, numerous TH-immunoreactive neurons contained Lewy bodies that were immunostained by antibody to TH. TH-immunoreactive neurons were decreased very markedly in the A2 regions of two patients with OH, and three patients without OH showed fairly marked decreases in the C1 or A2 region. In contrast, the number of TH-immunoreactive neurons in ALS was the same as in normal subjects. In MSA and some PD patients, orthostatic hypotension may partly be due to the involvement of the medullary catecholaminergic neurons. The lability of blood pressure in ALS probably is not related to the medullary catecholaminergic neurons.
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PMID:Decrease of medullary catecholaminergic neurons in multiple system atrophy and Parkinson's disease and their preservation in amyotrophic lateral sclerosis. 854 51


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