| First Author | Chang EH | Year | 2009 |
| Journal | Neurobiol Aging | Volume | 30 |
| Issue | 3 | Pages | 407-19 |
| PubMed ID | 17719144 | Mgi Jnum | J:145814 |
| Mgi Id | MGI:3836109 | Doi | 10.1016/j.neurobiolaging.2007.07.006 |
| Citation | Chang EH, et al. (2009) Age-related influence of the HDL receptor SR-BI on synaptic plasticity and cognition. Neurobiol Aging 30(3):407-19 |
| abstractText | Dysregulated cholesterol metabolism is a major risk factor for atherosclerosis and other late-onset disorders, such as Alzheimer's disease. The scavenger receptor, class B, type I (SR-BI) is critical in maintaining the homeostasis of cholesterol and alpha-tocopherol. SR-BI binds high-density lipoproteins (HDL) and mediates the selective transfer of cholesteryl esters and alpha-tocopherol from circulating HDL to cells. SR-BI is also involved in reverse cholesterol transport from peripheral tissues into the liver. Previous studies using SR-BI genetic knockout mice indicated that the deletion of SR-BI resulted in an accelerated onset of atherosclerosis. We hypothesized that SR-BI-dependent lipid dysregulation might disrupt brain function leading to cognitive impairment. Here, we report that very old SR-BI knockout mice show deficient synaptic plasticity (long-term potentiation) in the CA1 region of the hippocampus. Very old SR-BI KO mice also display selective impairments in recognition memory and spatial memory. Thus, SR-BI influences neural and cognitive processes, a finding that highlights the contribution of cholesterol and alpha-tocopherol homeostasis in proper cognitive function. |
