This paper will focus on commonalities in the aetiology and pathology in five areas of @entity16 with illustrative examples of therapy. Possibilities of multimodal and neuroprotective therapies in @entity1 disease, employing currently available drugs and showing evidence of neuroprotective potential in animal models, are discussed. By definition, neuroprotection is an effect that may result in salvage, recovery or regeneration of the nervous system, its cells, structure and function. It is thought that there are many neurochemical modulators of nervous system damage. In @entity302 , excessive @entity2227 -mediated neurotransmission, impaired voltage sensitive sodium and @entity460 channel functioning, impaired @entity1246 -mediated inhibition and alterations in acid base balance, when set in motion, may trigger a cascade of events leading to @entity528 and cell death. @entity697 in response to an insult may lead to acute or delayed @entity528 , apoptotic cell death, @entity528 , @entity130 , and @entity5219 . Cell death in the CNS following injury can occur in the manner of apoptosis, @entity39 or hybrid forms. In general, @entity143 receptor and non- @entity143 receptor mediated @entity130 results in @entity179 along an apoptosis- @entity39 continuum. The effects of @entity528 depend on factors including the degree of brain maturity or site of the lesion. There is some evidence supporting the hypothesis that neuroprotection may be a practical and achievable target using drugs already available, at present employed only for limited indications. Using these drugs early in the disease, may save decades of development of new drugs, which would require evaluation in animal studies, and @entity1 clinical trials. New drugs would also need to be shown to be safe and acceptable, physiologically not detrimental to @entity1 and free from idiosyncratic adverse effects.

Neuroprotection and XXXX .

@entity1 :: ('9606', 'Species') :: ['humans', 'human'] @entity2227 :: ('CHEBI:29987', 'Chemical') :: ['glutamate'] @entity697 :: ('MESH:D000208', 'Disease') :: ['Acute and chronic nervous system damage'] @entity1246 :: ('MESH:D005680', 'Chemical') :: ['GABA'] @entity39 :: ('MESH:D009336', 'Disease') :: ['necrosis'] @entity16 :: ('MESH:D009422', 'Disease') :: ['neurological disease'] @entity5219 :: ('MESH:D005911', 'Disease') :: ['gliosis'] @entity179 :: ('MESH:D019636', 'Disease') :: ['neurodegeneration'] @entity302 :: ('MESH:D004827', 'Disease') :: ['epilepsy'] @entity460 :: ('MESH:D002118', 'Chemical') :: ['calcium'] @entity143 :: ('CHEBI:6121', 'Chemical') :: ['NMDA'] @entity528 :: ('MESH:D009410', 'Disease') :: ['neuronal damage', 'neuronal death', 'neuronal injury', 'neuronal degeneration'] @entity130 :: ('MESH:D014947', 'Disease') :: ['excitotoxic injury', 'injury and loss']
@entity179 :: (MESH:D019636,Disease) :: ['neurodegenerative disease']
