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Retinal amyloid peptides and complement factor H in transgenic models of Alzheimer's disease

Alexandrov, Peter N.a; Pogue, Aileenb; Bhattacharjee, Surjyadiptab; Lukiw, Walter J.b

doi: 10.1097/WNR.0b013e3283497334

Murine transgenic models of Alzheimer's disease (Tg-AD) have been useful to analyze the contribution of β-amyloid precursor protein (βAPP), Aβ42 peptide deposition, and the proinflammatory mechanisms that characterize Alzheimer-type neuropathology. In this report, we have studied the levels of βAPP, Aβ40 and Aβ42 peptide, as well as the innate immune and inflammatory response-regulator complement factor H in the brain and retina in four different Tg-AD models including Tg2576, PSAPP, 3xTg-AD, and 5xFAD. Aged, symptomatic 5xFAD mice showed the highest retinal abundance of Aβ42 peptides and the highest deficits in complement factor H. This may be a useful model to study the mechanisms of amyloid-mediated inflammatory degeneration. The superior colliculus and retina obtained from late-stage Alzheimer's disease revealed upregulated amyloidogenic and inflammatory signaling along the anteroposterior axis of the retinal-primary visual cortex pathway.

aRussian Academy of Medical Sciences, Moscow, Russia

bLSU Neuroscience Center and Department of Ophthalmology, Louisiana State University Health Sciences Center, New Orleans, Louisiana, USA

Correspondence to Walter J. Lukiw, MS, PhD, LSU Neuroscience Center of Excellence, Louisiana State University Health Sciences Center, 2020 Gravier Street, Suite 904, New Orleans, LA 70112-2272, USA Tel: +1 504 599 0842; fax: +1 504 568 5801; e-mail:

Received April 27, 2011

Accepted June 2, 2011

© 2011 Lippincott Williams & Wilkins, Inc.