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

Amyloid (mycology) Proinflammatory cytokine
DOI: 10.1097/wnr.0b013e3283497334 Publication Date: 2016-04-25T16:57:07Z
ABSTRACT
Murine transgenic models of Alzheimer's disease (Tg-AD) have been useful to analyze the contribution β-amyloid precursor protein (βAPP), Aβ42 peptide deposition, and proinflammatory mechanisms that characterize Alzheimer-type neuropathology. In this report, we studied levels βAPP, Aβ40 peptide, as well innate immune inflammatory response-regulator complement factor H in brain retina four different Tg-AD including Tg2576, PSAPP, 3xTg-AD, 5xFAD. Aged, symptomatic 5xFAD mice showed highest retinal abundance peptides deficits H. This may be a model study amyloid-mediated degeneration. The superior colliculus obtained from late-stage revealed upregulated amyloidogenic signaling along anteroposterior axis retinal-primary visual cortex pathway.
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