scholarly journals Microglial Scavenger Receptors and Their Roles in the Pathogenesis of Alzheimer's Disease

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Kim Wilkinson ◽  
Joseph El Khoury

Alzheimer’s disease (AD) is increasing in prevalence with the aging population. Deposition of amyloid-β(Aβ) in the brain of AD patients is a hallmark of the disease and is associated with increased microglial numbers and activation state. The interaction of microglia with Aβappears to play a dichotomous role in AD pathogenesis. On one hand, microglia can phagocytose and clear Aβ, but binding of microglia to Aβalso increases their ability to produce inflammatory cytokines, chemokines, and neurotoxic reactive oxygen species (ROS). Scavenger receptors, a group of evolutionally conserved proteins expressed on the surface of microglia act as receptors for Aβ. Of particular interest are SCARA-1 (scavenger receptor A-1), CD36, and RAGE (receptor for advanced glycation end products). SCARA-1 appears to be involved in the clearance of Aβ, while CD36 and RAGE are involved in activation of microglia by Aβ. In this review, we discuss the roles of various scavenger receptors in the interaction of microglia with Aβand propose that these receptors play complementary, nonredundant functions in the development of AD pathology. We also discuss potential therapeutic applications for these receptors in AD.

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Francisca Cornejo ◽  
Rommy von Bernhardi

It is widely accepted that cells serving immune functions in the brain, namely, microglia and astrocytes, are important mediators of pathological phenomena observed in Alzheimer’s disease. However, it is unknown how these cells initiate the response that results in cognitive impairment and neuronal degeneration. Here, we review the participation of the immune response mediated by glial cells in Alzheimer’s disease and the role played by scavenger receptors in the development of this pathology, focusing on the relevance of class A scavenger receptor (SR-A) for Aβclearance and inflammatory activation of glial cell, and as a potential target for Alzheimer’s disease therapy.


2019 ◽  
Vol 72 (1) ◽  
pp. 191-197 ◽  
Author(s):  
Ping-Song Chou ◽  
Meng-Ni Wu ◽  
Chen-Cheng Yang ◽  
Cheng-Ting Shen ◽  
Yuan-Han Yang

1998 ◽  
Vol 95 (6) ◽  
pp. 555-558 ◽  
Author(s):  
Akinori Takeda ◽  
Takeshi Yasuda ◽  
Toshio Miyata ◽  
Yoji Goto ◽  
Masakazu Wakai ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Kelly N. Z. Fuller ◽  
Edwin R. Miranda ◽  
John P. Thyfault ◽  
Jill K. Morris ◽  
Jacob M. Haus

Although there is evidence for metabolic dysfunction and chronic inflammation in Alzheimer’s disease (AD), circulating levels of soluble receptor for advanced glycation end products (sRAGE) and the receptor for advanced glycation end products (RAGE) ligand S100B have not been characterized. sRAGE is an important mediator in disease as it can act as a ligand decoy for RAGE and attenuate downstream inflammatory signaling. Cognitively healthy elderly and AD participants with and without type 2 diabetes (n=135) were stratified according to the clinical dementia rating (CDR; 0 = normal cognition (NC); ≥0.5 = AD). Total serum sRAGE, endogenous secretory RAGE (esRAGE), and S100B were assayed via ELISAs, and cleaved RAGE (cRAGE) and the cRAGE : esRAGE ratio were calculated. cRAGE : esRAGE was lower in AD compared to NC (p<0.05). Metabolic substratifications were used to investigate the factors that influence sRAGE pathology in AD. Stratification by BMI classification, median fat mass, median HOMA-IR, median insulin, and median amylin were all metabolic or anthropometric factors which significantly interacted with sRAGE profiles within AD subjects. There were no significant differences in serum S100B between groups. These characterizations of sRAGE contribute evidence to the link between impaired metabolism and cognitive decline due to AD.


2009 ◽  
Vol 118 (3) ◽  
pp. 381-389 ◽  
Author(s):  
Michelle Y. Wang ◽  
Fred N. Ross-Cisneros ◽  
Divya Aggarwal ◽  
Chiao-Ying Liang ◽  
Alfredo A. Sadun

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