APOE 4 polymorphism results in early cognitive deficits in an EAE model.
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.
Department of Neurology, Barrow Neurological Institute, 500 W Thomas Road, Phoenix, AZ 85013, USA.
Jiang-long
JL
Tu
Chong-bo
CB
Zhao
Timothy
T
Vollmer
Stephen
S
Coons
Hao-jie
HJ
Lin
Stephen
S
Marsh
David M
DM
Treiman
Jiong
J
Shi
D000818:Animals; D030801:Animals, Genetically Modified; D053327:Apolipoprotein E4 / Q000235:genetics*; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D003072:Cognition Disorders / Q000201:enzymology / Q000235:genetics*; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000201:enzymology / Q000503:physiopathology*; D055786:Gene Knockout Techniques; D006624:Hippocampus / Q000201:enzymology; D006801:Humans; D008568:Memory; D009103:Multiple Sclerosis / Q000201:enzymology / Q000235:genetics*; D011110:Polymorphism, Genetic; D013037:Spatial Behavior
D053327:Apolipoprotein E4; D002795:Choline O-Acetyltransferase