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. Author manuscript; available in PMC: 2010 Mar 31.
Published in final edited form as: Neuroscience. 2009 Jan 19;159(3):1055–1069. doi: 10.1016/j.neuroscience.2009.01.023

Figure 8.

Figure 8

Neurovascular unit disruptions are seen in Alzheimer’s disease tissue. Panel A shows RNA expression levels of GFAP, aquaporin-4, Kir4.1, dystrophin 1 and Kv1.6 from AD tissue with mild, moderate and severe CAA. Data are shown as the average fold change vs. non-diseased control ± SEM. * indicates P<0.05, ** indicates P<0.01 compared to age-matched non-disease controls. Panels B–E show aquaporin-4 immunohistochemistry on human tissue sections from non-diseased brain (B), AD with mild CAA (C), AD with moderate CAA (D) and AD with severe CAA (E). 200× magnification, scale bar = 12.5µm.