title: Retinal amyloid peptides and complement factor H in transgenic models of Alzheimer's disease.
abstract: 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.
authors: Russian Academy of Medical Sciences, Moscow, Russia.
authors: Peter N
authors: PN
authors: Alexandrov
authors: Aileen
authors: A
authors: Pogue
authors: Surjyadipta
authors: S
authors: Bhattacharjee
authors: Walter J
authors: WJ
authors: Lukiw
mesh_terms: D000544:Alzheimer Disease / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000276:immunology* / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D017242:Complement Factor H / Q000276:immunology* / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic; D012160:Retina / Q000276:immunology* / Q000378:metabolism / Q000473:pathology
chemical_list: D016229:Amyloid beta-Peptides; D017242:Complement Factor H