作者: L. Genis , Y. Chen , E. Shohami , D.M. Michaelson
DOI: 10.1002/(SICI)1097-4547(20000515)60:4<559::AID-JNR15>3.0.CO;2-K
关键词:
摘要: Apolipoprotein E (apoE)-deficient mice have learning and memory impairments that are associated with specific neurochemical changes hyperphosphorylation of distinct epitopes the cytoskeletal protein tau. Furthermore, such highly susceptible to sequelae brain trauma their ability recover from head injury is impaired. In present study we investigated extent neuronal maintenance repair apoE-deficient related aberrations at tau phosphorylation level. This was pursued by subjecting control closed (CHI) examination, utilizing immunoblot assays, resulting effects on phosphorylation. The results thus obtained revealed hyperphosphorylated before CHI this insult in transient hyperphosphorylation, whose time course two mouse groups varied markedly. Tau injured controls maximal about 4 hr after reverted basal levels 24 hr. contrast, almost no injury-induced observed injury. Some hyper-phosphorylation detected head-injured longer intervals, but its markedly lower than values controls. These findings show chronic brought apoE deficiency acute response both same domain mount