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

被引：109

作者：

Alexandrov, Peter N. ^{[1
]}

Pogue, Aileen ^{[2
,3
]}

Bhattacharjee, Surjyadipta ^{[2
,3
]}

Lukiw, Walter J. ^{[2
,3
]}

机构：

[1] Russian Acad Med Sci, Moscow, Russia

[2] Louisiana State Univ, Hlth Sci Ctr, LSU Neurosci Ctr, New Orleans, LA 70112 USA

[3] Louisiana State Univ, Hlth Sci Ctr, Dept Ophthalmol, New Orleans, LA 70112 USA

来源：

NEUROREPORT | 2011年 / 22卷 / 12期

关键词：

5xFAD; age-related macular degeneration; Alzheimer's disease; inflammatory neurodegeneration; miRNA-146a; retina; Tg2576; transgenic models of Alzheimer's disease; NF-KAPPA-B; PRECURSOR-PROTEIN; ANIMAL-MODELS; MOUSE MODELS; BETA; PLAQUES; MICE; PRESENILIN-1; EXPRESSION; MUTANT;

D O I：

10.1097/WNR.0b013e3283497334

中图分类号：

Q189 [神经科学];

学科分类号：

071006 [神经生物学];

摘要：

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.

引用

页码：623 / 627

页数：5

共 25 条

[1]

Micro-RNA-128 (miRNA-128) down-regulation in glioblastoma targets ARP5 (ANGPTL6), Bmi-1 and E2F-3a, key regulators of brain cell proliferation [J].