Results 221 to 230 of about 171,447 (234)
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Neuroprotection by tetracyclines
Trends in Pharmacological Sciences, 2004The neuroprotective properties of tetracyclines have been clearly established in rodent models of acute and chronic neurodegeneration during the past few years. Recent findings have provided novel insights into the molecular and cellular mechanisms of protection of neurons and oligodendrocytes by tetracyclines.
Carlos Matute, María Domercq
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2003
The activation of adenosine A1, A2 andA3 receptors can protect neurones against damage generated by mechanical or hypoxic/ischaemic insults as well as excitotoxins. A1 receptors are probably effective by suppressing transmitter release and producing neuronal hyperpolarisation.
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The activation of adenosine A1, A2 andA3 receptors can protect neurones against damage generated by mechanical or hypoxic/ischaemic insults as well as excitotoxins. A1 receptors are probably effective by suppressing transmitter release and producing neuronal hyperpolarisation.
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BILOBALIDE AND NEUROPROTECTION
Pharmacological Research, 2002In vivo studies have indicated that systemically administered bilobalide, a sesquiterpene trilactone constituent of Ginkgo biloba leaf extracts, can reduce cerebral edema produced by triethyltin, decrease cortical infarct volume in certain stroke models, and reduce cerebral ischemia.
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2004
During the last years it has become obvious that the current way of treating epilepsy with antiepeileptic drugs is insufficient concerning the modification of the underlying disesease and provides merely a symptomatic treatment, without clear influence on the course of the disease.
Péter Halász, György Rásonyi
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During the last years it has become obvious that the current way of treating epilepsy with antiepeileptic drugs is insufficient concerning the modification of the underlying disesease and provides merely a symptomatic treatment, without clear influence on the course of the disease.
Péter Halász, György Rásonyi
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Neuroprotection in glaucoma: a model for neuroprotection in optic neuropathies
Current Opinion in Ophthalmology, 2003Efforts to discover modalities and pathophysiologies that might afford successful neurorescue, neurorestoration, and neuroprotection of cells of the central nervous system have focused on processes that affect the central nervous system proper, that is, the brain. Often overlooked in the search for neural protection is the fact that the mammalian optic
Barrett Katz +2 more
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Epilepsia, 2007
Summary Neuroprotection following status epilepticus should encompass not only the prevention of neuronal death, but also preservation of neuronal and network function. This is critical because these aims are not necessarily equivalent; prevention of neuronal loss, for example, does not inevitably prevent epileptogenesis.
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Summary Neuroprotection following status epilepticus should encompass not only the prevention of neuronal death, but also preservation of neuronal and network function. This is critical because these aims are not necessarily equivalent; prevention of neuronal loss, for example, does not inevitably prevent epileptogenesis.
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Phytoestrogens as neuroprotectants
Drugs of Today, 2009Recent large clinical trials demonstrating deleterious effects of postmenopausal hormone replacement therapy have raised interest in the use of food products and extracts containing phytoestrogens as potential safe alternatives for menopausal symptoms, age-related cognitive decline and neurodegenerative diseases.
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Australian & New Zealand Journal of Psychiatry, 2011
The case described by Dhillon and colleagues [1] underlines the importance of noting significant clinical events in single case studies as well as providing very important information about the imp...
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The case described by Dhillon and colleagues [1] underlines the importance of noting significant clinical events in single case studies as well as providing very important information about the imp...
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Excitotoxicity and Neuroprotection
The Journal of Clinical Psychiatry, 1997Issue: Excitatory neurotransmission is a normal physiologic process mediated by the neurotransmitter glutamate. Too much glutamate release can be destructive and literally excite a neuron to death in a process called excitotoxicity. Blocking this process may be neuroprotective and prevent brain disorders mediated by excitotoxicity.
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2017
Abstract Acute cerebral injury sets into motion a cascade of deleterious biochemical events that cause further neuronal damage and amplify deleterious effects. This cascade develops over time and potentially may be attenuated or limited by pharmacologic manipulation.
Stocchetti, Nino, Carbonara, Marco
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Abstract Acute cerebral injury sets into motion a cascade of deleterious biochemical events that cause further neuronal damage and amplify deleterious effects. This cascade develops over time and potentially may be attenuated or limited by pharmacologic manipulation.
Stocchetti, Nino, Carbonara, Marco
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