Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002736 (amyotrophic lateral sclerosis)
 19,048 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vimentin immunoreactivity was examined in brain tissues from non-neurological and various human central nervous system disease cases. In all brain tissues examined, vimentin immunoreactivity was intensely positive in ependymal cells and subpial tissues, and weakly positive in some capillaries and some white matter astrocytes. In affected areas of Alzheimer's disease (AD), Pick's disease, amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS) and cerebral infarction cases, numerous intensely vimentin-immunopositive astrocytes of both protoplasmic and fibrous morphology were demonstrated. A few such astrocytes were also observed in Parkinson's disease and progressive supranuclear palsy. ALS, MS and infarction brains also had numerous, strongly vimentin-positive, round and fat-laden microglia/macrophages. In AD and ALS, a few reactive microglia with irregularly enlarged shapes were vimentin positive. In AD, they were almost exclusively related to senile plaques.
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PMID:Vimentin immunoreactivity in normal and pathological human brain tissue. 152 71

Motor evoked potentials (MEPs) elicited by magnetic coil stimulation of motor cortex were studied at rest and during maximum voluntary muscle contraction in 20 normal subjects and 42 patients with motor disorders. MEP parameters employed in this study included: onset latency, amplitude, MEP/M wave amplitude ratio and background EMG/MEP area ratio. Maximum voluntary contraction increased the amplitude of MEPs compared to the size of M waves elicited by peripheral nerve stimulation. A reduced MEP/M wave amplitude ratio had a higher correlation with pyramidal tract involvement than did a prolonged MEP onset latency. Analysis of MEP parameters may help in the differential diagnosis of cerebral infarction, ALS and cervical spondylotic radiculomyelopathy. The inhibitory period which follows MEPs during voluntary contraction was observed in all subjects; the mean duration in normal subjects was 126.6 +/- 29.5 msec. The mean duration of the inhibitory period in patients with cerebral infarction, ALS and cervical spondylotic radiculomyelopathy was 73.9 +/- 41.7 msec, 79.5 +/- 54.5 msec and 85.1 +/- 36.5 msec, respectively. These values were significantly shorter than in normal subjects.
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PMID:Motor potentials evoked by magnetic stimulation of the motor cortex in normal subjects and patients with motor disorders. 171 18

The possible role of trace elements in a pathogenesis of central nervous system (CNS) on degenerative and demyelinating diseases has been suggested. Simultaneous measurements of Zinc (Zn) and iron (Fe) concentration in CNS were undertaken by neutron activation analysis in CNS tissues: a patient with multiple sclerosis (MS), five patients with amyotrophic lateral sclerosis (ALS), five with spinocerebellar degeneration (SCD), and five with cerebral infarction (CVD) in non-invasive area of CNS as control. Although Zn and Fe concentration were present in white matter and gray matter of CNS in each disease, 1) Zn concentration showed no special pattern in gray matter among four diseases, but decreased more in white matter of MS and ALS than that of CVD (p less than 0.05); 2) Fe concentration in gray matter of SCD increased more than that in CVD (p less than 0.05), but Fe concentration in white matter of CVD was increased more than that of ALS (p less than 0.05); 3) Fe concentration of CNS in a patient with MS was not notable except for high Fe concentration in caudate nucleus and globus pallidus. The demyelinated pathological area in CNS of MS showed a decrease in Zn level but no change in Fe level. These results indicate that low Zn concentration in CNS tissues of MS seemed to be responsible for CNS demyelination, but not for undernutrition due to poor conditions of a patient with MS. It seems that Zn might be one pathogenetic factor of MS, but the action of Fe in MS can not be ruled out.
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PMID:[Zinc concentration in the central nervous system in a case of multiple sclerosis--comparison with other neurological diseases]. 179 99

Onuf's nucleus is a small motoneuron group in S2 anterior horn, which was described by Onufrowicz in 1900. He suggested that the motoneurons in the nucleus innervated striated muscles involved in election and ejaculation. The nucleus is readily shown by the K-B stain on account of its pale staining background which is sharply demarcated from the surrounding network of fine myelinated fibers. However, neuropathological descriptions of the nucleus are very rare. Pons-Tortella et al reported the sparing of this nucleus in acute anterior poliomyelitis. In 1977. We reported that Onuf's nucleus were well preserved in cases with ALS, in which the function of bladder and rectal sphincters is often intact until the latest stage of the illness. On the control , Shy-Drager syndrome showed severe degeneration of Onuf's nucleus. The patients with Shy-Drager syndrome showed clinically evident urinary and/or fecal incontinence. Combination of these clinical and pathological findings led to conclusion that Onuf's nucleus innervates the striated muscles of the sphincters. In 1990, Iwatsubo et al studied corticofugal projections to the motoneurons with Nauta-Gygax's technique in a patient with cerebral infarction. They verified that the oculomotor and abducens nuclei and Onuf's nucleus do not receive direct cortical projections. These motoneurons are characteristically spared in ALS. For the studies on ALS, it is important to know what differences between Onuf's nucleus and other motoneuron groups in anterior horn are biochemically and physiologically.
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PMID:[Neuropathology of Onuf's nucleus]. 181 91

Widespread astrogliosis exists in the subcortical white matter in amyotrophic lateral sclerosis (ALS). As revealed by glial fibrillary acidic protein (GFAP) immunostaining, the gliosis has the morphological properties of an active process. It is present in the midfrontal, inferior parietal, temporal, cingulate, and occipital cortices, as well as in the motor cortex. Compared to matched regions from other neurological diseases, the gliosis in ALS does not appear to be the nonspecific result of a progressive, degenerative disease. In cell number and apparent cell size, the gliosis is comparable to that present in neurological diseases known to have white matter gliosis. Cytologically, the gliosis most closely resembles that present in cases of cerebral infarction. The basis for this similarity is unknown.
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PMID:Reactive astrogliosis is widespread in the subcortical white matter of amyotrophic lateral sclerosis brain. 177 89

Human liver carboxylesterase (CE) is an enzyme capable of metabolizing drugs, and may also function as a regulator of lipid metabolism. We examined one isoform of CE by immunohistochemistry in the brains of neurologically normal, Alzheimer disease (AD), amyotrophic lateral sclerosis (ALS) and cerebral infarction cases. In all but the infarcted brains, the anti-CE antibody stained only capillary endothelial cells in the brain and spinal cord tissues. In infarct brain areas, intense immunoreactivity of the macrophages was seen. In contrast, the macrophages in the ALS lateral columns and the reactive microglia located in the center of classical senile plaques in AD, as well as other reactive microglial cells in the grey matter, showed no immunoreactivity. In the central nervous system, CE may function as a protective factor against foreign chemicals in capillary endothelial cells, and the antibody to CE may serve as a marker for invading macrophages from the systemic circulation.
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PMID:Immunohistochemistry with an antibody to human liver carboxylesterase in human brain tissues. 783 38

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 examined serum antibodies to 4 species of fucogangliosides: fucosyl-GM1, fucosyl-GD1b, alpha galactosyl (alpha fucosyl) GM1 and alpha galactosyl (alpha fucosyl) GD1b, in 329 patients with various neurologic diseases, 32 patients with non-neurologic autoimmune diseases and 50 healthy persons. Nine patients with Guillain-Barre syndrome, 2 with amyotrophic lateral sclerosis and 2 with cerebral infarction had IgG anti-fucosyl-GM1 antibody. Five patients with Guillain-Barre syndrome, 1 with cerebral infarction and 1 normal control subject had IgM anti-fucosyl-GM1 antibody, 3 of whom also had IgG anti-fucosyl-GM1 antibody. Sixteen of 17 patients who had IgG or IgM antibody to fucosyl-GM1 showed no sensory dysfunction. Yoshino et al. [J. Neurochem. 1993, 61: 658-663] speculated that anti-fucosyl-GM1 antibody functions in the development of sensory neuropathy, but our results do not support this. Two patients with sensory ataxic neuropathy had high IgM antibody titers to fucosyl-GD1b and alpha galactosyl (alpha fucosyl) GD1b. These fucogangliosides may be the target molecules for serum antibodies in some patients with sensory ataxic neuropathy.
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PMID:Antibodies to fucogangliosides in neurological diseases. 926 Aug 62

Using the multi-shot EPI method we investigated the clinical application of diffusion weighted imaging (DWI) in the diagnosis of neurological disease. The multi-shot method provided better susceptibility artifact-free DWI than the single-shot method particularly in the region of the posterior cranial fossa. DWI using the multi-shot EPI method readily shows the pyramidal tract extending from the internal capsule to the brainstems which is inaccessible by the conventional single-shot EPI method, and providing three-dimensional and distinct images of pyramidal tract changes in amyotrophic lateral sclerosis or cerebral infarction with pyramidal tract disturbance. Our findings suggest that the use of DWI with the multi-shot EPI method would provide a technique for the easy diagnosis and evaluation of various neurological diseases.
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PMID:[Clinical application of multi-shot diffusion EPI in neurological disease]. 980 94

We determined the cerebrospinal fluid (CSF) levels of adenosine, a mediator of cerebral blood flow regulation, and neopterin, a macrophage-producing compound, in patients with neurological disorders. Compared to control subjects, the adenosine levels were significantly increased in the patients with acute-stage cerebral infarction (n=12, p<0.0001), acute meningitis (n=10, p<0.0001), or amyotrophic lateral sclerosis (ALS, n=12, p<0.05) (Mann-Whitney U-test). The neopterin levels were significantly increased in the 41 patients with human T-lymphotropic virus type I-associated myelopathy/tropical spastic paraparesis (HAM/TSP, p<0.0001), acute meningitis (p<0.0001), ALS (p<0.05) (Mann-Whitney U-test), or acute-stage cerebral infarction (p<0.005, Student's t-test). In the analysis of 41 HAM/TSP patients, the neopterin levels were significantly correlated with the cell number and glucose levels in the CSF, and were a sensitive marker of inflammation. Several of the HAM/TSP patients with increased adenosine levels were probably complicated with other diseases. The increased neopterin levels in the HAM/TSP group persisted, suggesting that the mononuclear cellular infiltration remained for a long time.
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PMID:Adenosine and neopterin levels in cerebrospinal fluid of patients with neurological disorders. 1022 68


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