Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1998-12-18
pubmed:abstractText
The beta-amyloid peptides, A beta1-42 and A beta1-40, were quantified in ventricular CSF taken daily for up to 3 weeks from six individuals with severe traumatic brain injury (TBI). There was considerable interindividual variability in the levels of A beta peptides, but in general A beta1-42 levels equalled or exceeded those of A beta1-40. Averaging the daily totals of our trauma cohort revealed that the levels of A beta1-42 and A beta1-40 rose after injury, peaking in the first week and then declining toward control levels over the next 2 weeks. A beta1-42 levels were on average two to three times higher in the trauma cohort than in CSF from nontrauma samples. Compared with nontrauma samples, the A beta1-40/A beta1-42 ratio decreased about fivefold in the trauma patients, further indicative of increased A beta1-42 levels. The ratio remained low at all time points studied. No change was measured in the levels of beta-amyloid precursor protein during the same interval. These results suggest that A beta1-42 becomes elevated in the CSF after severe brain trauma.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0022-3042
pubmed:author
pubmed:issnType
Print
pubmed:volume
71
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2505-9
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Traumatic brain injury increases beta-amyloid peptide 1-42 in cerebrospinal fluid.
pubmed:affiliation
Neuroscience Therapeutics, Parke-Davis Pharmaceutical Research Division, Warner-Lambert Company, Ann Arbor, Michigan 48105, USA.
pubmed:publicationType
Journal Article