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Publication : APOE 4 polymorphism results in early cognitive deficits in an EAE model.

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.
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