Journal
EXPERIMENTAL AND MOLECULAR MEDICINE
Volume 46, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/emm.2013.147
Keywords
Alzheimer's disease; astrocyte; cortex; hippocampus; mice; receptor for advanced glycation end products (RAGE)
Funding
- Inter-Institutional Collaboration Research Program - Korea Research Council of Fundamental Science & Technology (KRCF) [Kiom-2010-2]
- Korea Research Foundation Grant - Korean Government [KRF-2010-0023880]
- National Research Council of Science & Technology (NST), Republic of Korea [kiom-2010-2] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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The receptor for advanced glycation end products (RAGE) has been reported to have a pivotal role in the pathogenesis of Alzheimer's disease (AD). This study investigated RAGE levels in the hippocampus and cortex of a triple transgenic mouse model of AD (3xTg-AD) using western blotting and immunohistochemical double-labeling to assess cellular localization. Analysis of western blots showed that there were no differences in the hippocampal and cortical RAGE levels in 10-month-old adult 3xTg-AD mice, but significant increases in RAGE expression were found in the 22- to 24-month-old aged 3xTg-AD mice compared with those of age-matched controls. RAGE-positive immunoreactivity was observed primarily in neurons of aged 3xTg-AD mice with very little labeling in non-neuronal cells, with the notable exception of RAGE presence in astrocytes in the hippocampal area CA1. In addition, RAGE signals were co-localized with the intracellular amyloid precursor protein (APP)/amyloid beta (Ab) but not with the extracellular APP/A beta. In aged 3xTg-AD mice, expression of human tau was observed in the hippocampal area CA1 and co-localized with RAGE signals. The increased presence of RAGE in the 3xTg-AD animal model showing critical aspects of AD neuropathology indicates that RAGE may contribute to cellular dysfunction in the AD brain.
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