Skip to main content
. 2004 Feb 23;101(9):3100–3105. doi: 10.1073/pnas.0308724101

Fig. 2.

Fig. 2.

Neuronal insulin resistance causes Tau hyperphosphorylation in vivo. (A) Western blot analysis of brain extracts derived from individual randomly fed mice with antibodies against Akt or pAkt (Ser-473). (Lower) The densitometric quantification as mean ± SEM [control (open bars) and NIRKO (filled bars) mice] of at least eight animals of each genotype is shown (**, P < 0.01 by unpaired Student's t test). (B) Western blot analysis of brain extracts derived from individual randomly fed mice with antibodies against GSK3β or pGSK3β (Ser-9). (Lower) The densitometric quantification as mean ± SEM [control (open bars) and NIRKO (filled bars) mice] of at least eight animals of each genotype (**, P < 0.01 by unpaired Student's t test). (C) Immunohistochemistry of layer V of the frontal cortex (Left) and the pyramidal cells of the CA1 region of the hippocampus (Right) with antiserum specific for pGSK3β (4′,6-diamidino-2-phenylindole counterstaining). (D) Immunoblotting of protein extracts from whole brain lysates of control and NIRKO mice with the AT180 (paired helical filament-Tau phosphorylated at Thr-231) and AT8 (paired helical filament-Tau phosphorylated at Ser-202) antibodies. Data represent mean ± SEM [control (open bars) and NIRKO (filled bars) mice] of at least six animals of each genotype (**, P < 0.01 unpaired Student's t test).