Linked Life Data

8123218

Source:http://linkedlifedata.com/resource/pubmed/id/8123218

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1994-4-14
pubmed:abstractText
Alcoholism is often associated with brain damage and cognitive deficits. Because drinking patterns can include periods of alcohol consumption followed by abstinence, binge drinking may enhance the possibility of brain damage. Chronic administration of ethanol leads to upregulation of N-methyl-D-aspartate (NMDA) and calcium receptors and increased release of glucocorticoids. NMDA-mediated mechanisms and glucocorticoid actions on the hippocampus are associated with brain damage. Thus, ethanol withdrawal may make the brain more vulnerable to damage from these mechanisms, especially with binge drinking. Therapeutic adjuncts for treating ethanol withdrawal, including NMDA, calcium, and glucocorticoid antagonists, may eventually prove useful in preventing further brain damage in alcoholism.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0741-8329
pubmed:author
pubmed:issnType
Print
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
559-61
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:articleTitle
Are binge drinkers more at risk of developing brain damage?
pubmed:affiliation
Neurosciences and Behavioral Research Branch, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20857-0001.
pubmed:publicationType
Journal Article, Review