Increased expression of the receptor for advanced glycation end products in neurons and astrocytes in a triple transgenic mouse model of Alzheimer's disease.
- Author:
Bo Ryoung CHOI
1
;
Woo Hyun CHO
;
Jiyoung KIM
;
Hyong Joo LEE
;
Chihye CHUNG
;
Won Kyung JEON
;
Jung Soo HAN
Author Information
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords: Alzheimer's disease; astrocyte; cortex; hippocampus; mice; receptor for advanced glycation end products (RAGE)
- MeSH: Advanced Glycosylation End Product-Specific Receptor; Alzheimer Disease/genetics/*metabolism; Amyloid beta-Peptides/metabolism; Animals; Astrocytes/*metabolism; CA1 Region, Hippocampal/growth & development/metabolism/pathology; Humans; Mice; Mice, Transgenic; Neurons/*metabolism; Receptors, Immunologic/genetics/*metabolism; tau Proteins/genetics/metabolism
- From:Experimental & Molecular Medicine 2014;46(2):e75-
- CountryRepublic of Korea
- Language:English
- Abstract: 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 (Abeta) but not with the extracellular APP/Abeta. 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.
