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. Author manuscript; available in PMC: 2011 Dec 1.

Published in final edited form as: J Neuropathol Exp Neurol. 2010 Dec;69(12):1201–1209. doi: 10.1097/NEN.0b013e3181fd252c

Fig. 8 — Immunolocalization of aquaporin 1 (AQP1), aquaporin 4 (AQP 4) and β-amyloid (Aβ) plaques in Alzheimer disease + cerebral amyloid angiopathy (AD + CAA). (A-C) AQP1 (A) and AQP4 (B) immunoreactivity (IR) appears to be in a plaque-like distribution that corresponds to Aβ IR (C). (D, E) AQP4 IR in a patient with AD with no CAA also shows IR in a plaque-like distribution. (Original magnifications: A, C, 10x; D, 20x; E, 40x).

Fig. 8 — Immunolocalization of aquaporin 1 (AQP1), aquaporin 4 (AQP 4) and β-amyloid (Aβ) plaques in Alzheimer disease + cerebral amyloid angiopathy (AD + CAA). (A-C) AQP1 (A) and AQP4 (B) immunoreactivity (IR) appears to be in a plaque-like distribution that corresponds to Aβ IR (C). (D, E) AQP4 IR in a patient with AD with no CAA also shows IR in a plaque-like distribution. (Original magnifications: A, C, 10x; D, 20x; E, 40x).