| First Author | Tu JL | Year | 2009 |
| Journal | Biochem Biophys Res Commun | Volume | 384 |
| Issue | 4 | Pages | 466-70 |
| PubMed ID | 19422789 | Mgi Jnum | J:150595 |
| Mgi Id | MGI:3851054 | Doi | 10.1016/j.bbrc.2009.04.153 |
| Citation | Tu JL, et al. (2009) APOE 4 polymorphism results in early cognitive deficits in an EAE model. Biochem Biophys Res Commun 384(4):466-70 |
| abstractText | Recent clinical studies have identified an association between APOE 4 and cognitive deficits in patients with multiple sclerosis. We induced experimental autoimmune encephalomyelitis (EAE) in APOE knockout (KO) and human APOE 4 knockin (E4) mice to study the interaction of APOE and neuroinflammation on cognition. After EAE induction, KO and E4 showed significant deficits in spatial learning and recall. Regional decreases in choline acetyltransferase localized to the hippocampus. Induction of EAE in a transgenic APOE animal provides a template from which we can decipher the role APOE has on cognition in the context of neuroinflammation. |