Linked Life Data

11462776

Source:http://linkedlifedata.com/resource/pubmed/id/11462776

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2001-7-20
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0077-8923
pubmed:author
pubmed:issnType
Print
pubmed:volume
939
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
238-53
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Synaptic deprivation and age-related vulnerability to hypoxic-ischemic neuronal injury. A hypothesis.
pubmed:affiliation
Departments of Neurology and Neuroscience, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.
pubmed:publicationType
Journal Article