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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Neuroinflammation
2016 ; 13
(1
): 56
Nephropedia Template TP
gab.com Text
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English Wikipedia
The blockage of the Nogo/NgR signal pathway in microglia alleviates the formation
of A? plaques and tau phosphorylation in APP/PS1 transgenic mice
#MMPMID26939570
Fang Y
; Yao L
; Li C
; Wang J
; Wang J
; Chen S
; Zhou XF
; Liao H
J Neuroinflammation
2016[Mar]; 13
(1
): 56
PMID26939570
show ga
BACKGROUND: Alzheimer's disease (AD) is characterized by extracellular ?-amyloid
(A?) plaques, neurofibrillary tangles (NFTs), and microglia-dominated
neuroinflammation. The Nogo/NgR signal pathway is involved in AD pathological
features, but the detailed mechanism needs further investigation. Our previous
studies have confirmed that the activation of NgR on microglia by Nogo promotes
the expression of proinflammatory cytokines and inhibits cell adhesion and
migration behaviors. In the present study, we investigated the effects of
Nogo/NgR signaling pathway on the pathological features of AD and possible
mechanisms. METHODS: After NEP1-40 (a competitive antagonist of Nogo/NgR pathway)
was intracerebroventricularly administered via mini-osmotic pumps for 2 months in
amyloid precursor protein (APP)/PS1 transgenic mice, plaque load, tau
phosphorylation, and inflammatory responses were determined. After primary mouse
neurons were exposed to the conditioned medium from BV-2 microglia stimulated by
Nogo, the production of A? and phosphorylation of tau was quantified by ELISA and
western blot. RESULTS: Inhibition of the Nogo/NgR signaling pathway ameliorated
pathological features including amyloid plaques and phosphorylated levels of tau
in APP/PS1 mice. In addition, after treatment with the conditioned medium from
BV-2 microglia stimulated by Nogo, A? production and tau phosphorylation in
cultured neurons were increased. The conditioned medium also increased the
expression of APP, its amyloidogenic processing, and the activity of GSK3? in
neurons. The conditioned medium was also proinflammatory medium, and the blockage
of the Nogo/NgR pathway improved the neuroinflammatory environment in APP/PS1
mice. CONCLUSIONS: Taken together, the neuroinflammation mediated by Nogo/NgR
pathway in microglia could directly take part in the pathological process of AD
by influencing the amyloidogenesis and tau phosphorylation. These results
contribute to a better understanding of AD pathogenesis and could offer a new
therapeutic option for delaying the progression of AD.
|Amyloid beta-Peptides/*metabolism
[MESH]
|Amyloid beta-Protein Precursor/metabolism
[MESH]
|Animals
[MESH]
|Culture Media, Conditioned
[MESH]
|Inflammation/pathology/prevention & control
[MESH]