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Title: Depletion of microglia ameliorates white matter injury and cognitive impairment in a mouse chronic cerebral hypoperfusion model
Authors: Kakae, Masashi
Tobori, Shota
Morishima, Misa
Nagayasu, Kazuki
Shirakawa, Hisashi
Kaneko, Shuji
Author's alias: 抱, 将史
白川, 久志
金子, 周司
Keywords: Chronic cerebral hypoperfusion
Cognitive impairment
White matter injury
Colony-stimulating factor 1
Issue Date: 5-Jul-2019
Publisher: Elsevier B.V.
Journal title: Biochemical and Biophysical Research Communications
Volume: 514
Issue: 4
Start page: 1040
End page: 1044
Abstract: Microglia are immune cells in the central nervous system (CNS) and essential for homeostasis that are important for both neuroprotection and neurotoxicity, and are activated in a variety of CNS diseases. Microglia aggravate cognitive impairment induced by chronic cerebral hypoperfusion, but their precise roles under these conditions remain unknown. Here, we used PLX3397, a colony-stimulating factor 1 receptor inhibitor, to deplete microglia in mice with chronic cerebral hypoperfusion induced by bilateral common carotid artery stenosis (BCAS). Cognitive impairment induced 28 days after BCAS was significantly improved in mice fed a diet containing PLX3397. In PLX3397-fed mice, microglia were depleted and white matter injury induced by BCAS was suppressed. In addition, the expression of proinflammatory cytokines, interleukin 6 and tumor necrosis factor alpha, was suppressed in PLX3397-fed mice. Taken together, these findings suggest that microglia play destructive roles in the development of cognitive impairment and white matter injury induced by chronic cerebral hypoperfusion. Thus, microglia represent a potential therapeutic target for chronic cerebral hypoperfusion-related diseases.
Rights: © 2019. This manuscript version is made available under the CC-BY-NC-ND 4.0 license
The full-text file will be made open to the public on 5 July 2020 in accordance with publisher's 'Terms and Conditions for Self-Archiving'.
This is not the published version. Please cite only the published version. この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。
DOI(Published Version): 10.1016/j.bbrc.2019.05.055
PubMed ID: 31097227
Appears in Collections:Journal Articles

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