Skip to main content
. Author manuscript; available in PMC: 2013 Oct 17.
Published in final edited form as: J Immunol. 2010 Apr 5;184(9):5333–5343. doi: 10.4049/jimmunol.0903382

Fig 2. Significant attenuation of amyloid deposition in mIFNγ expressing (P2→5mo) TgCRND8 mice.

Fig 2

A-H. rAAV1-mIFNγ or rAAV1-EGFP was injected into the cerebral ventricles of TgCRND8 mice on neonatal day P2 and sacrificed after 5 months (P2→5mo). mIFNγ expressing TgCRND8 mice (A, C-E) were analyzed along with age-matched EGFP expressing mice (B, F-H, Control). Representative sections of the whole brain (A-B) as well as hippocampus (C-H) from 3 mice from each group is shown following pan Aβ immunostaining. Scale Bar, 600µm (A-B), 150µm (C-H). n=10–12/group).

I-J. Image analysis of amyloid plaque immunoreactivity shows a significant decrease in Aβ plaque burdens in the forebrain (I) and hippocampus (J) of mIFNγ expressing mice compared to EGFP expressing control mice (n=10–12/group, *p<0.05).

K-L. Biochemical analyses of Aβ42 and Aβ40 levels in P2→5 month old mIFNγ expressing TgCRND8 mice compared to EGFP expressing age matched controls. Both SDS-soluble and SDS-insoluble (FA fraction) Aβ42 and Aβ40 levels in the forebrain of mIFNγ injected mice were significantly reduced compared to control mice (n=10/group, *p<0.05 and **p<0.05).