| pubmed-article:11462776 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11462776 | lifeskim:mentions | umls-concept:C0175677 | lld:lifeskim |
| pubmed-article:11462776 | lifeskim:mentions | umls-concept:C0521390 | lld:lifeskim |
| pubmed-article:11462776 | lifeskim:mentions | umls-concept:C0871712 | lld:lifeskim |
| pubmed-article:11462776 | lifeskim:mentions | umls-concept:C0679109 | lld:lifeskim |
| pubmed-article:11462776 | lifeskim:mentions | umls-concept:C1512571 | lld:lifeskim |
| pubmed-article:11462776 | pubmed:dateCreated | 2001-7-20 | lld:pubmed |
| pubmed-article:11462776 | pubmed:abstractText | Advanced age is associated with physiological changes, such as cerebral autoregulation dysfunction, atrial fibrillation, reduced cerebral blood flow, elevated blood pressure, and other changes. Stroke-related dementia is associated with brain loss principally due to strokes, and neuropathological examination of the brains of old people shows a direct correlation between the extent of brain loss and dementia. However, the exact mechanism of the age related vulnerability to hypoxic-ischemic neuronal injury remains unknown. The majority of synapses in the brain use excitatory amino acids as their neurotransmitter. Glutamate, a major endogenous excitatory amino acid required for normal physiological excitation, is also involved in the pathophysiology of hypoxic-ischemic neuronal injury. The N-methyl-D-aspartate (NMDA) glutamate receptor subtype plays a major role in mediating hypoxic-ischemic neuronal injury. NMDA receptors also mediate adaptive responses important for synaptic plasticity. This report explores the possible role of synaptic activity as a protective mechanism against neuronal cell death. Specifically, the role of NMDA receptors in neuronal plasticity by upregulating a survival pathway is discussed. Loss of a neuronal population that uses glutamate as its neurotransmitter leads to a loss of activity on the postsynaptic neurons or synaptic deprivation. Deprivation of excitatory amino acids on the postsynaptic neurons results in the failure of activity-dependent induced intrinsic survival pathways induced by NMDA receptors. The loss of neuroprotective intrinsic survival pathways increases the vulnerability of these neurons to more hypoxic-ischemic neuronal damage. Since cerebral infarction is also age related, this hypothesis provides a plausible explanation of how we become more vulnerable to hypoxic-ischemic neuronal injury as a function of age. | lld:pubmed |
| pubmed-article:11462776 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11462776 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11462776 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11462776 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11462776 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11462776 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11462776 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11462776 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11462776 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11462776 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11462776 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:11462776 | pubmed:issn | 0077-8923 | lld:pubmed |
| pubmed-article:11462776 | pubmed:author | pubmed-author:ChoiJJ | lld:pubmed |
| pubmed-article:11462776 | pubmed:author | pubmed-author:MariniA MAM | lld:pubmed |
| pubmed-article:11462776 | pubmed:author | pubmed-author:LabuttaRR | lld:pubmed |
| pubmed-article:11462776 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11462776 | pubmed:volume | 939 | lld:pubmed |
| pubmed-article:11462776 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11462776 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11462776 | pubmed:pagination | 238-53 | lld:pubmed |
| pubmed-article:11462776 | pubmed:dateRevised | 2003-11-14 | lld:pubmed |
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| pubmed-article:11462776 | pubmed:meshHeading | pubmed-meshheading:11462776... | lld:pubmed |
| pubmed-article:11462776 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11462776 | pubmed:articleTitle | Synaptic deprivation and age-related vulnerability to hypoxic-ischemic neuronal injury. A hypothesis. | lld:pubmed |
| pubmed-article:11462776 | pubmed:affiliation | Departments of Neurology and Neuroscience, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA. | lld:pubmed |
| pubmed-article:11462776 | pubmed:publicationType | Journal Article | lld:pubmed |
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