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Traumatic Brain Injury Increases β-Amyloid Peptide 1-42 in Cerebrospinal Fluid
Authors:Charlotte A. Raby,Maria C. Morganti-Kossmann,Thomas Kossmann,Philip F. Stahel,M. Desiree Watson,Lori M. Evans,&dagger  Pankaj D. Mehta,Katharyn Spiegel,&Dagger  Yu-Min Kuo,&Dagger  Alex E. Roher, Mark R. Emmerling
Affiliation:Neuroscience Therapeutics, Parke-Davis Pharmaceutical Research Division, Warner-Lambert Company, Ann Arbor, Michigan;; New York Institute for Basic Research, Staten Island, New York;; Haldeman Laboratory for Alzheimer's Disease Research, Sun Health Research Institute, Sun City, Arizona, U.S.A.;and; Division of Trauma Surgery, Department of Surgery, University Hospital, Zürich, Switzerland
Abstract:Abstract: The β-amyloid peptides, Aβ1-42 and Aβ1-40, 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 Aβ peptides, but in general Aβ1-42 levels equalled or exceeded those of Aβ1-40. Averaging the daily totals of our trauma cohort revealed that the levels of Aβ1-42 and Aβ1-40 rose after injury, peaking in the first week and then declining toward control levels over the next 2 weeks. Aβ1-42 levels were on average two to three times higher in the trauma cohort than in CSF from nontrauma samples. Compared with nontrauma samples, the Aβ1-40/Aβ1-42 ratio decreased about fivefold in the trauma patients, further indicative of increased Aβ1-42 levels. The ratio remained low at all time points studied. No change was measured in the levels of β-amyloid precursor protein during the same interval. These results suggest that Aβ1-42 becomes elevated in the CSF after severe brain trauma.
Keywords:Alzheimer's disease    β-Amyloid precursor protein    Risk factors    Brain    CSF    Head trauma    Injury
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