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

Murine transgenic models of Alzheimer's disease (Tg-AD) have been useful to analyze the contribution of beta-amyloid precursor protein (beta APP), A beta 42 peptide deposition, and the proinflammatory mechanisms that characterize Alzheimer-type neuropathology. In this report, we have studied the levels of beta APP, A beta 40 and A beta 42 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 A beta 42 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. NeuroReport 22:623-627 (C) 2011 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.