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glutamate dehydrogenase/atrofija
Nuoroda įrašoma į mainų sritį
Puslapis 1 nuo 88 rezultatus
Glutamate dehydrogenase deficiency in cerebellar degenerations: clinical, biochemical and molecular genetic aspects.
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Glutamate dehydrogenase (GDH), an enzyme central to glutamate metabolism, is significantly reduced in patients with heterogenous neurological disorders characterized by multiple system atrophy (MSA) and predominant involvement of the cerebellum and its connections. In human brain, GDH exists in
Normal cerebellar glutamate dehydrogenase protein in spinocerebellar degeneration.
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Immunochemical analyses (Western blots) of cerebellar homogenates for glutamate dehydrogenase (GDH) from patients with spinocerebellar degeneration and control subjects were conducted. Four patients with autosomal dominant Joseph disease type of spinocerebellar degeneration, one patient with
Glutamate dehydrogenase deficiency in patients with olivopontocerebellar atrophy.
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Deficiency of glutamate dehydrogenase appears to be associated with a chronic progressive degenerative disorder manifesting parkinsonian extrapyramidal features, ataxia, supranuclear oculomotor dysfunction, a peripheral neuropathy and, in some cases, amyotrophy. The clinical features resemble those
Glutamate dehydrogenase deficiency in spinocerebellar degenerations.
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Glutamate dehydrogenase (GDH) activity in leukocytes and platelets in spinocerebellar degenerations (SCD) was determined. In the same subject, GDH activity was higher and more reproducible in platelets than in leukocytes. GDH was decreased significantly in olivopontocerebellar atrophy (OPCA) (Ca.
Pathology of olivopontocerebellar atrophy with glutamate dehydrogenase deficiency.
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We report the neuropathologic findings in the first patient with recognized glutamate dehydrogenase (GDH) deficiency to come to postmortem examination. He had progressive cerebellar ataxia beginning at age 21. He died at age 47 of pulmonary emboli. Postmortem examination revealed pancerebellar,
Glutamate dehydrogenase and its isozyme activity in olivopontocerebellar atrophy.
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Evaluation of glutamate dehydrogenase (GDH) in 12 patients with olivopontocerebellar atrophy showed deficiency of the enzyme in the group as well as in each patient. The activity of total GDH was 77.7% of that in controls. We also demonstrated two components of this enzyme differentiated by their
Multiple system degeneration with glutamate dehydrogenase deficiency: pathology and biochemistry.
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The neuropathological findings in a patient with antemortem diagnosis of olivopontocerebellar atrophy (OPCA) and reduced leucocytic glutamate dehydrogenase (GDH) activity included cerebellar cortical degeneration, most marked in the superior vermis, mild atrophy of the pons and the inferior olivary
Glutamate dehydrogenase in olivopontocerebellar atrophies: leukocytes, fibroblasts, and muscle mitochondria.
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Glutamate dehydrogenase (GDH) activity was 68% of control values in leukocyte homogenates of 11 patients with dominant olivopontocerebellar atrophies (OPCA) and 46% in muscle mitochondria of 4 patients with dominant OPCA. In three patients with recessive OPCA and in one sporadic patient, muscle GDH
Neurophysiologic study of olivopontocerebellar atrophy with or without glutamate dehydrogenase deficiency.
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By neurophysiologic investigations, we evaluated 20 patients with olivopontocerebellar atrophy (OPCA), comprising 8 with glutamate dehydrogenase (GDH) deficiency and 12 with normal GDH activity. We found sensorimotor, predominantly sensory axonal neuropathy distally in the legs, and peripheral
Low leukocyte glutamate dehydrogenase activity does not correlate with a particular type of multiple system atrophy.
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Leucocyte glutamate dehydrogenase (GDH) activity was measured in 26 normal control subjects, 20 patients with multiple system atrophy presenting features of either olivopontocerebellar atrophy or striatonigral degeneration and in a heterogenous group of 15 patients with spinocerebellar
Partially deficient glutamate dehydrogenase activity and attenuated oscillatory potentials in patients with spinocerebellar degeneration.
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Glutamate dehydrogenase (GDH, EC 1.4.1.2) catalyzes the synthesis and degradation of glutamate, an excitatory neurotransmitter in the retina. Recently, two forms of GDH, a soluble heat-stable form and a particulate heat-labile form, have been demonstrated to be deficient in some types of
Glutamate metabolism of leukocytes and skin fibroblasts in spinocerebellar degeneration with lowered glutamate dehydrogenase activity.
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From 21 patients with spinocerebellar degeneration 5 had markedly decreased glutamate dehydrogenase (GDH) activities and high values of serum plasma glutamate level after oral glutamate loading tests. Skin fibroblasts from patients with GHD deficiency showed intracellularly higher glutamate and
Abnormal platelet glutamate dehydrogenase activity and activation in dominant and nondominant olivopontocerebellar atrophy.
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Glutamate dehydrogenase (GDH) activity and its allosteric modulation by purine nucleotides were studied in platelet preparations from 4 patients with a nondominant form of adult-onset olivopontocerebellar atrophy (OPCA) and in affected and nonaffected members of two families with a dominant form of
Decreased glutamate dehydrogenase protein in spinocerebellar degeneration.
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A radioimmunoassay system for determining content of glutamate dehydrogenase (GDH) in human leukocytes was established and studied in 14 patients with spinocerebellar ataxia or atypical Parkinsonism. The protein content of leukocyte GDH was decreased in four patients and the reduction in the protein
[Glutamate dehydrogenase and its isozyme activity in spinocerebellar degeneration].
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