| Title | Ameliorating Alzheimer's-like Pathology by Minocycline via Inhibiting Cdk5/p25 Signaling |
| Author | |
| Corresponding Author | Zhao, Yu; Cai, Zhiyou |
| Publication Years | 2022
|
| DOI | |
| Source Title | |
| ISSN | 1570-159X
|
| EISSN | 1875-6190
|
| Volume | 20Issue:9 |
| Abstract | Background: Minocycline has multiple neuroprotective roles in abundant brain diseases, including the prevention and treatment of Alzheimer's disease (AD). Cdk5/p25 signaling plays an important role in the onset and development of Alzheimer's-like pathology. The aim of the present work was to further explore the underlying mechanism which minocycline effects on Cdk5/p25 signaling related to Alzheimer's-like pathology. Methods: The cognitive function of animals was measured by the Morris water maze test. The levels of A beta were determined by an enzyme-linked immunosorbent assay. The levels of APP, beta- and gamma-secretases, and the biomarkers of tau (total tau and hyperphosphorylated tau), inflammatory cytokine and matrix metalloproteinases (MMP-2 and MMP-9), and biomarkers of synapse and Cdk5/p25 signaling, were detected by the Western blotting. The biomarkers of the synapse, inflammatory cytokine, and matrix metalloproteinases (MMP-2 and MMP-9) were also determined by immunofluorescence. Results: Minocycline improved learning and memory in APP/PS1 mice. It limited the production of A beta and hyperphosphorylation of tau in the hippocampus and ameliorated synaptic deficit. Moreover, it also inhibited the activation of Cdk5/p25 signaling, inflammation, and matrix metalloproteinases. Conclusion: Minocycline mitigates Alzheimer's-like pathology via limiting the activation of Cdk5/p25 signaling pathway and improves cognitive deficits. |
| Keywords | |
| URL | [Source Record] |
| Indexed By | |
| Language | English
|
| SUSTech Authorship | First
; Corresponding
|
| Funding Project | Chongqing Natural Science Foundation[cstc2018jcyjA4051]
; Chongqing Health and Natural Science Foundation[2018ZDXM004]
; Natural Science Foundation of Hubei Province[2015 CFB260]
; Hubei Province Health and Family Planning Scientific Research Project[WJ2015MB219]
; Shiyan Natural Science Foundation[15K70]
|
| WOS Research Area | Neurosciences & Neurology
; Pharmacology & Pharmacy
|
| WOS Subject | Neurosciences
; Pharmacology & Pharmacy
|
| WOS Accession No | WOS:000843817800012
|
| Publisher | |
| Data Source | Web of Science
|
| Citation statistics |
Cited Times [WOS]:3
|
| Document Type | Journal Article |
| Identifier | http://kc.sustech.edu.cn/handle/2SGJ60CL/394236 |
| Department | The Third People's Hospital of Shenzhen 南方科技大学第一附属医院 |
| Affiliation | 1.Southern Univ Sci & Technol, Shenzhen Peoples Hosp 3, Affiliated Hosp 2, Dept Neurol, 29 Bulan Rd, Shenzhen 518112, Guangdong, Peoples R China 2.Univ Chinese Acad Sci, Chongqing Gen Hosp, Dept Neurol, 312 Zhongshan First Rd, Chongqing 400013, Peoples R China 3.Chongqing Key Lab Neurodegenerat Dis, Chongqing 400013, Peoples R China 4.Hubei Univ Med, Renmin Hosp, Shiyan Renmin Hosp, Dept Neurol, Shiyan 442000, Hubei, Peoples R China |
| First Author Affilication | The Third People's Hospital of Shenzhen; Shenzhen People's Hospital |
| Corresponding Author Affilication | The Third People's Hospital of Shenzhen; Shenzhen People's Hospital |
| First Author's First Affilication | The Third People's Hospital of Shenzhen; Shenzhen People's Hospital |
| Recommended Citation GB/T 7714 |
Zhao, Yu,Wang, Chuanling,He, Wenbo,et al. Ameliorating Alzheimer's-like Pathology by Minocycline via Inhibiting Cdk5/p25 Signaling[J]. Current Neuropharmacology,2022,20(9).
|
| APA |
Zhao, Yu,Wang, Chuanling,He, Wenbo,&Cai, Zhiyou.(2022).Ameliorating Alzheimer's-like Pathology by Minocycline via Inhibiting Cdk5/p25 Signaling.Current Neuropharmacology,20(9).
|
| MLA |
Zhao, Yu,et al."Ameliorating Alzheimer's-like Pathology by Minocycline via Inhibiting Cdk5/p25 Signaling".Current Neuropharmacology 20.9(2022).
|
| Files in This Item: | There are no files associated with this item. | |||||
Items in the repository are protected by copyright, with all rights reserved, unless otherwise indicated.
;
Edit Comment