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. Author manuscript; available in PMC: 2009 Aug 1.
Published in final edited form as: Nat Cell Biol. 2008 Dec 21;11(2):143–153. doi: 10.1038/ncb1819

Figure 5.

Figure 5

SRF gene transfer to pial arteries reduces Aβ pathology in AD models. (a) Aβ immunostaining in transduced pial vessels (upper panels) and focally in brain tissue (lower panels) after expression of a control vector (Ad.shGFP) or Ad.shSRF in 24-month-old Dutch/Iowa APP mice. Scale bars,50 µm. (b, c) Aβ load in transduced pial vessels (b) and focally in brain (c) after adenoviral-mediated transfer of shGFP or shSRF in 24-month-old Dutch/Iowa APP mice. (d, e) Amyloid load in transduced pial vessels (d) and focal Aβ40 and Aβ42 levels in brain (e) after adenoviral-mediated transfer of shGFP and shSRF in 24-month-old Dutch/Iowa APP mice. (f) The levels of SREBP2, immature LRP (LRP 600 band) and mature LRP (LRP 85 band) in pial vessels after overexpression of shGFP and shSRF in 24-month-old Dutch/Iowa APP mice. Graphs show relative band density, compared with β-actin. (g) 2-photon in vivo longitudinal imaging of amyloid with methoxy-XO4 and Texas Red dextran angiography in the cortical lamina I in 16-month-old APPsw± mice transduced locally in the pial vessels with either Ad.shGFP or Ad.shSRF. Scale bars, 100 µm. Graphs show XO4 relative signal intensity. (h) Aβ40 and Aβ42 focal brain levels in the areas containing pial vessels transduced with Ad.shGFP or Ad.shSRF in 16-month-old APPsw± mice. Data represent mean ± s.e.m. of 5 animals per group (b–d, f–h).