Results 171 to 180 of about 46,918 (224)

Excitotoxicity in the Pathogenesis of Autism

Neurotoxicity Research, 2012
Autism is a debilitating neurodevelopment disorder characterised by stereotyped interests and behaviours, and abnormalities in verbal and non-verbal communication. It is a multifactorial disorder resulting from interactions between genetic, environmental and immunological factors.
M M, Essa, N, Braidy, K R, Vijayan, S, Subash, G J, Guillemin   +4 more
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Excitotoxicity

Molecular Neurobiology, 1994
Neurochemical observations on cortical biopsies form 48 patients under surgical treatment for pharmacoresistant partial epilepsy showed a 70-80% increase in glutamate concentration when expressed in relation to neuron specific enolase. Intraperitoneal administration of one of its receptor agonists, kainic acid (KA), to the rat led to increased ...
K G, Haglid, S, Wang, Y, Qiner, A, Hamberger   +3 more
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Apoptosis, Excitotoxicity, and Neuropathology

Experimental Cell Research, 1998
While a high rate of cell loss is tolerated and even required to model the developing nervous system, an increased rate of cell death in the adult nervous system underlies neurodegenerative disease. Evolutionarily conserved mechanisms involving proteases, Bcl-2-related proteins, p53, and mitochondrial factors participate in the modulation and execution
M, Leist, P, Nicotera
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Excitotoxicity in the Brain

1998
Excitotoxins are a special group of neurotoxic substances that excite somatic and dendritic receptors in such a way that the neurons may die. All excitotoxins are in principle agonists of glutamate receptors in the brain and are structurally related to glutamate.
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Alternative excitotoxic hypotheses

Neurology, 1992
The concept of excitotoxicity, neuronal death produced by overstimulation of excitatory amino acid receptors, has become a popular way of explaining the pathogenesis of neuronal death in a variety of acute and chronic neurologic diseases. While there is strong evidence supporting the role of excitotoxicity in acute processes such as hypoxia/ischemia ...
R L, Albin, J T, Greenamyre
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Pathophysiology of oligodendroglial excitotoxicity

Journal of Neuroscience Research, 1996
Oligodendrocyte-like cells (OLD) derived from the rat oligodendroglial precursor line, CG-4, express Ca(2+)-permeable non-methyl-D-aspartate glutamate receptor channels (GluR). Exposure to kainate, an L-glutamate analogue, markedly elevates OLC Ca2+ influx and cytosolic [Ca2+], and results in damage to both OLC plasma membrane and OLC nuclear DNA.
A, Yoshioka, B, Bacskai, D, Pleasure
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Excitotoxicity in Aging and Dementia

1983
The extracellular concentration of glutamate in the neocortex of human brain may-increase progressively with ageing. Glutamergic nerve terminals seem to be a major source of the amino acid. There is no evidence that the concentration of extracellular glutamate is increased in the neocortex in Alzheimer’s disease.
D. M. Bowen, C. C. T. Smith, A. N. Davison   +2 more
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Calcium, ischemia and excitotoxicity

Cell Calcium, 2010
The initial reports regarding a cytotoxic role of calcium ions were published over 30 years ago. In neurons, calcium ions can gain entry into the cell through several mechanisms. These include the over-activation of glutamate receptors (NMDA, AMPA, KA) or of a range of channels and transporters (TRPM2, TRPM7, NCX, ASICs, CaV1.2, and hemichannels ...
Kinga, Szydlowska, Michael, Tymianski
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Excitotoxic mechanisms in the pathogenesis of dementia

Neurochemistry International, 1994
Alzheimer disease and related dementias, in common with most major neurological diseases, are characterized by localized brain damage. An abundance of senile plaques and neurofibrillary tangles in certain brain areas is pathognomic of the disease: of the two, the density of tangles may correlate more closely with disease severity ante mortem.
Dodd, PR, Scott, HL, Westphalen, RI
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Excitotoxicity in neonatal hypoxia

Mental Retardation and Developmental Disabilities Research Reviews, 2001
AbstractHypoxic‐ischemic encephalopathy (HIE) in neonates is a disorder of excessive neuronal excitation that includes seizures, abnormal EEG activity, and delayed failure of oxidative metabolism with elevated levels of lactic acid in the brain. Evidence from experimental models and clinical investigation indicates that HIE is triggered by a profound ...
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