Asset Details
Do you wish to reserve the book?
The adhesion and migration of microglia to β-amyloid (Aβ) is decreased with aging and inhibited by Nogo/NgR pathway
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
The adhesion and migration of microglia to β-amyloid (Aβ) is decreased with aging and inhibited by Nogo/NgR pathway
Do you wish to request the book?
The adhesion and migration of microglia to β-amyloid (Aβ) is decreased with aging and inhibited by Nogo/NgR pathway
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
The adhesion and migration of microglia to β-amyloid (Aβ) is decreased with aging and inhibited by Nogo/NgR pathway
2018
Overview
Background
Alzheimer’s disease is characterized by progressive accumulation of β-amyloid (Aβ)-containing amyloid plaques, and microglia play a critical role in internalization and degradation of Aβ. Our previous research confirmed that Nogo-66 binding to Nogo receptors (NgR) expressed on microglia inhibits cell adhesion and migration in vitro.
Methods
The adhesion and migration of microglia isolated from WT and APP/PS1 mice from different ages were measured by adhesion assays and transwells. After NEP1-40 (a competitive antagonist of Nogo/NgR pathway) was intracerebroventricularly administered via mini-osmotic pumps for 2 months in APP/PS1 transgenic mice, microglial recruitment toward Aβ deposits and CD36 expression were determined.
Results
In this paper, we found that aging led to a reduction of microglia adhesion and migration to fAβ
1–42
in WT and APP/PS1 mice. The adhesion and migration of microglia to fAβ
1–42
were downregulated by the Nogo, which was mediated by NgR, and the increased inhibitory effects of the Nogo could be observed in aged mice. Moreover, Rho GTPases contributed to the effects of the Nogo on adhesion and migration of microglia to fAβ
1–42
by regulating cytoskeleton arrangement. Furthermore, blocking the Nogo/NgR pathway enhanced recruitment of microglia toward Aβ deposits and expression of CD36 in APP/PS1 mice.
Conclusion
Taken together, Nogo/NgR pathway could take part in Aβ pathology in AD by modulating microglial adhesion and migration to Aβ and the Nogo/NgR pathway might be an important target for treating AD.
Publisher
BioMed Central,BioMed Central Ltd,Springer Nature B.V,BMC
Subject
/ Aging
/ Alzheimer Disease - genetics
/ Alzheimer Disease - pathology
/ Amyloid beta-Peptides - pharmacology
/ Amyloid beta-Protein Precursor - genetics
/ Animals
/ Biomedical and Life Sciences
/ cdc42 GTP-Binding Protein - metabolism
/ Cell Adhesion - drug effects
/ Cell Movement - drug effects
/ Enzymes
/ Humans
/ Kinases
/ Memory
/ Mice
/ Myelin Proteins - pharmacology
/ Nogo
/ Peptide Fragments - pharmacology
/ rac1 GTP-Binding Protein - metabolism
/ rhoA GTP-Binding Protein - metabolism
/ Rodents
