aspartic acid/atrofia

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Degeneration of cholinergic neurons in the basal nucleus following kainic or N-methyl-D-aspartic acid application to the cerebral cortex in the rat.

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The effect on cholinergic neurons in the basal nucleus of exposing the cortex to excitotoxic amino acids was examined in the rat. Kainic or N-methyl-D-aspartic acid were applied extradurally over the cerebral cortex of one side. This resulted in a severe depletion in the numbers of neurons in the

Collagen turnover in normal and degenerate human intervertebral discs as determined by the racemization of aspartic acid.

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Knowledge of rates of protein turnover is important for a quantitative understanding of tissue synthesis and catabolism. In this work, we have used the racemization of aspartic acid as a marker for the turnover of collagen obtained from healthy and pathological human intervertebral disc matrices. We

Role of inducible nitric oxide synthase in N-methyl-d-aspartic acid-induced strio-nigral degeneration.

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N-Methyl-d-aspartate (NMDA)-induced striatal excitotoxicity is mediated by nitric oxide (NO) but the role of inflammatory mechanisms and inducible nitric oxide synthase (iNOS) induction is not clear. Unilateral intrastriatal administration of NMDA to rats resulted in the loss of intrinsic striatal

Involvement of matrix metalloproteinases in capillary degeneration following NMDA-induced neurotoxicity in the neonatal rat retina.

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Interactions between neuronal cells and vascular cells in the retina are critical for maintaining retinal tissue homeostasis. Impairment of cellular interactions contributes to development and progression of retinal diseases. Previous studies demonstrated that neuronal cell damage leads to capillary

Decreased Expression of DREAM Promotes the Degeneration of Retinal Neurons.

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The intrinsic mechanisms that promote the degeneration of retinal ganglion cells (RGCs) following the activation of N-Methyl-D-aspartic acid-type glutamate receptors (NMDARs) are unclear. In this study, we have investigated the role of downstream regulatory element antagonist modulator (DREAM) in

The Purkinje cell degeneration 5J mutation is a single amino acid insertion that destabilizes Nna1 protein.

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In the mouse, Purkinje cell degeneration (pcd) is a recessive mutation characterized by degeneration of cerebellar Purkinje cells, retinal photoreceptors, olfactory bulb mitral neurons, and certain thalamic neurons, and is accompanied by defective spermatogenesis. Previous studies of pcd have led to

Pathogenic CWF19L1 variants as a novel cause of autosomal recessive cerebellar ataxia and atrophy.

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Autosomal recessive cerebellar ataxia (ARCA) is a group of neurological disorders characterized by degeneration or abnormal development of the cerebellum and spinal cord. ARCA is clinically and genetically highly heterogeneous, with over 20 genes involved. Exome sequencing of a girl with ARCA from

Is aspartic acid the neurotransmitter of the perforant pathway?

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In order to determine whether an amino acid may act as a neurotransmitter in the perforant pathway we examined the effect of lesion of rat entorhinal cortex on the concentrations of various amino acids in the hippocampus proper and fascia dentata. Only the aspartic acid content was found

Infrared and laser Raman spectral studies of bis(dl-aspartic acid) sulfate.

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The infrared and Raman spectra of bis(dl-aspartic acid) sulfate in the crystalline state are recorded at room temperature and the vibrational assignments of the observed wavenumbers are made. The presence of two carbonyl (CO) groups has been identified in the title complex and the two carbonyl

[Present possibilities of age determination in forensic medicine with emphasis on the importance of measurement of D- and L- forms of aspartic acid. I. An overview].

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Evaluation of age of unknown deceased persons belongs to the most important ways to identification. For the time being, morphological methods are used, namely evaluation of age according to Gustafson's method from tooth grindings or by macroscopical estimation of abrasion, transparency of root

Aspartic acid repeat polymorphism of the asporin gene with susceptibility to osteoarthritis of the knee in a Korean population.

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Osteoarthritis (OA) is a common disease that is characterized by the degeneration of joint cartilage in the knee, hip and hand. Recently, it has been reported that susceptibility to OA is affected by the number of aspartic acid (D) residues in the amino-terminal of the asporin protein. In order to

Contribution of N-methyl-DL-aspartic acid (NMDA)-sensitive neurons to generating oscillatory potentials in Royal College of Surgeons rats.

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OBJECTIVE We investigated how the N-methyl-DL-aspartic acid (NMDA) receptor contributes to generating oscillatory potentials (OPs) of the electroretinogram (ERG) in the Royal College of Surgeons (RCS) rat. METHODS Scotopic ERGs were recorded from dystrophic and wild-type congenic (WT) RCS rats (n =

Free amino acid concentrations in blood cells of two brothers with gyrate atrophy of the choroid and retina with hyperornithinaemia.

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In this study we selected blood cells as accessible tissues and measured the free amino acid concentrations in erythrocytes, lymphocytes, and granulocytes of two patients with gyrate atrophy with hyperornithinaemia. We found that ornithine concentrations were elevated in blood cells, to different

Nur7 is a nonsense mutation in the mouse aspartoacylase gene that causes spongy degeneration of the CNS.

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Aspartoacylase (ASPA) is an oligodendrocyte-restricted enzyme that catalyzes the hydrolysis of neuronally derived N-acetylaspartate (NAA) to acetate and aspartic acid. ASPA deficiency leads to the fatal childhood autosomal recessive leukodystrophy Canavan disease (CD). Here we demonstrate that the

Structural model of the OPA1 GTPase domain may explain the molecular consequences of a novel mutation in a family with autosomal dominant optic atrophy.

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Autosomal dominant optic atrophy (ADOA) is the most frequent hereditary optic neuropathy. Three loci have been reported for ADOA: a major locus, harboring all identified mutations to date, maps to 3q28 (OPA1), a second locus is linked to 18q12.2-q12.3 (OPA4) and a third locus on 22q12.1-q13.1 (OPA5)

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