| Title | Simvastatin therapy prevents brain trauma-induced increases in beta-amyloid peptide levels. | | Author(s) | Abrahamson EE, Ikonomovic MD, Dixon CE, DeKosky ST | | Institution | Department of Neurology, Brain Trauma Research Center, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. | | Source | Ann Neurol 2009 Sep; 66(3):407-14. | | MeSH | Alzheimer Disease
Amyloid beta-Protein
Animals
Behavior, Animal
Brain Injuries
Disease Models, Animal
Hippocampus
Humans
Maze Learning
Mice
Neuroprotective Agents
Postural Balance
Risk Factors
Simvastatin
Tissue Distribution
| | Abstract | Elevations in beta-amyloid peptide (A beta) levels after traumatic brain injury (TBI) may confer risk for developing Alzheimer's disease in head trauma patients. We investigated the effects of simvastatin, a 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor, on hippocampal A beta burden in a clinically relevant head injury/intervention model using mice expressing human A beta. Simvastatin therapy blunted TBI-induced increases in A beta, reduced hippocampal tissue damage and microglial activation, and improved behavioral outcome. The ability of statins to reduce post-injury A beta load and ameliorate pathological sequelae of brain injury makes them potentially effective in reducing the risk of developing Alzheimer's disease in TBI patients. | | Language | eng | | Pub Type(s) | Journal Article
Research Support, N.I.H., Extramural
| | PubMed ID | 19798641 |
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