O4-02-05: Lower microglial Fcγ RI/II and macrophage scavenger receptor a in human Alzheimer's disease after Aβ42 immunisation.

2011 ◽  
Vol 7 ◽  
pp. S684-S685
Author(s):  
Elina Zotova ◽  
Clive Holmes ◽  
James Neal ◽  
Seth Love ◽  
James Nicoll ◽  
...  
2018 ◽  
Vol 69 ◽  
pp. 336-350 ◽  
Author(s):  
Francisca Cornejo ◽  
Marianne Vruwink ◽  
Claudia Metz ◽  
Paola Muñoz ◽  
Nicole Salgado ◽  
...  

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.


Biochemistry ◽  
2009 ◽  
Vol 48 (50) ◽  
pp. 11858-11871 ◽  
Author(s):  
Claudine Neyen ◽  
Annette Plüddemann ◽  
Pietro Roversi ◽  
Benjamin Thomas ◽  
Lei Cai ◽  
...  

2006 ◽  
Vol 84 (4) ◽  
pp. 874-890 ◽  
Author(s):  
Kenji Nakamura ◽  
Wakana Ohya ◽  
Hiroshi Funakoshi ◽  
Gaku Sakaguchi ◽  
Akira Kato ◽  
...  

2006 ◽  
Vol 7 (3) ◽  
pp. 514
Author(s):  
C. Neyen ◽  
A. Plüddemann ◽  
B. Thomas ◽  
A. Akoulitchev ◽  
L. Cai ◽  
...  

2008 ◽  
Vol 38 (11) ◽  
pp. 3068-3079 ◽  
Author(s):  
Thomas Areschoug ◽  
Johan Waldemarsson ◽  
Siamon Gordon

2020 ◽  
Author(s):  
Jahirul Islam ◽  
Jung-Ah Cho ◽  
Ju-yong Kim ◽  
Kyung-Sun Park ◽  
Young-Jae koh ◽  
...  

Abstract Amyloid β (Aβ) and/or ATP activates NLRP3 inflammasome (N3I) by P2 × 7R ion channel of microglia, which is crucial in neuroinflammation shown in Alzheimer’s disease (AD). Due to polymorphisms, subtypes, and ubiquitous expression of P2 × 7R, inhibition of P2 × 7R has not been effective for AD. We first report that GPCR19 is a prerequisite for P2 × 7R-mediated N3I activation and Taurodeoxycholate (TDCA), a GPCR19 ligand, inhibited the priming phase of N3I activation, suppressed P2 × 7R expression and P2 × 7R-mediated Ca++ mobilization, and N3I oligomerization which is essential for production of IL-1β/IL-18. Further, TDCA increased expression of scavenger receptor (SR) A, enhanced phagocytosis of Aβ, and decreased Aβ plaque numbers in the brain of 5x Familial Alzheimer’s disease (5xFAD) mice. TDCA also reduced microgliosis, prevented neuronal loss, and improved memory function of 5xFAD mice. The pleiotropic roles of GPCR19 in P2 × 7-mediated N3I activation suggest that targeting GPCR19 might resolve neuroinflammation in AD patients.


Diabetes ◽  
2007 ◽  
Vol 56 (2) ◽  
pp. 363-372 ◽  
Author(s):  
Hitomi Kataoka Usui ◽  
Kenichi Shikata ◽  
Motofumi Sasaki ◽  
Shinichi Okada ◽  
Mitsuhiro Matsuda ◽  
...  

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