Lesley M. Foley1, Eric E. Abrahamson2,
T. Kevin Hitchens1,3, Chien Ho1,3, William R. Paljug2,
John A. Melick4, Patrick M. Kochanek4,5, Milos D.
Ikonomovic2
1Pittsburgh NMR Center for
Biomedical Research, Carnegie Mellon University, Pittsburgh, PA, United
States; 2Department of Neurological Surgery, University of
Pittsburgh School of Medicine, Pittsburgh, PA, United States; 3Department
of Biological Sciences, Carnegie Mellon University, Pittsburgh, PA, United
States; 4Safar Center for Resuscitation Research, University of
Pittsburgh School of Medicine, Pittsburgh, PA, United States; 5Departments
of Critical Care Medicine, Pediatrics & Anesthesiology, University of
Pittsburgh School of Medicine, Pittsburgh, PA, United States
Amyloid precursor protein and its toxic metabolite amyloid- (A) increase after TBI. It is unknown whether increases in A after TBI contributes to changes in brain hemodynamics. We used ASL-MRI to evaluate regional cerebral blood flow (CBF) in wild type C57BL/6 and APPNLh/NLh/C57BL/6 mice that express the human A (hA) peptide. Both at 72 hr and 3 weeks after injury, CBF deficits were significantly greater in APPNLh/NLh/C57BL/6 mice. Increased hA concentrations may contribute to impaired hemodynamics and prolonged deficits in recovery of perfusion, supporting the idea that TBI is a risk factor for developing Alzheimers disease later in life.
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