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Dulaglutide ameliorates STZ induced AD-like impairment of learning and memory ability by modulating hyperphosphorylation of tau and NFs through GSK3β
Zhou M, Chen S, Peng P, Gu Z, Yu J, Zhao G, Deng Y.. Biochemical and biophysical research communications, 2019-02-14
Topic: Gut, metabolism and diet
Plain-language summary
Dulaglutide, a novel long-acting glucagon-like peptide 1 (GLP-1) receptor agonist, is an incretin mimetic approved for type 2 diabetes mellitus (T2DM) treatment. Alzheimer's disease (AD) is called type 3 diabetes. The aim of this study is to explore the effects of dulaglutide on the learning and memory impairment in AD mice induced by injection of streptozocin (STZ) via intracerebroventricularly (i.c.v.). 32 male C57/BL6 mice were randomly divided into four groups: control group (CON); AD model group (STZ); dulaglutide treated (Dul); dulaglutide and exendin(9-39) (Ex). Western blotting was used to detect the levels of phosphorylated tau, neurofilament (NFs) proteins and phosphorylated PI3K/AKT/GSK3β signaling pathway. Morris water maze (MWM) test was used to assess the spatial learning and memory ability. The results displayed that the hyperphosphorylation of tau and NFs were increased in the STZ and Ex groups compared to the control and Dul groups. Dulaglutide also significantly shortened the escape latency and increased the number of hidden platform crossings in MWM test. The effects of dulaglutide on decreasing the hyperphosphorylation of tau and NFs proteins through improving the PI3K/AKT/GSK3β signaling pathway may be related to its protective effects on impairment of AD-like learning and memory.
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APA 7th
Zhou, M., Chen, S., Peng, P., Gu, Z., Yu, J., Zhao, G., et al. (2019). Dulaglutide ameliorates STZ induced AD-like impairment of learning and memory ability by modulating hyperphosphorylation of tau and NFs through GSK3β. Biochemical and biophysical research communications. https://doi.org/10.1016/j.bbrc.2019.01.103
Vancouver
Zhou M, Chen S, Peng P, Gu Z, Yu J, Zhao G, et al. Dulaglutide ameliorates STZ induced AD-like impairment of learning and memory ability by modulating hyperphosphorylation of tau and NFs through GSK3β. Biochemical and biophysical research communications. 2019. doi:10.1016/j.bbrc.2019.01.103. PMID: 30773255.
BibTeX
@article{zhou2019-30773255,
author = {Zhou, M. and Chen, S. and Peng, P. and Gu, Z. and Yu, J. and Zhao, G. and Deng, Y.},
title = {{Dulaglutide ameliorates STZ induced AD-like impairment of learning and memory ability by modulating hyperphosphorylation of tau and NFs through GSK3β}},
journal = {Biochemical and biophysical research communications},
year = {2019},
doi = {10.1016/j.bbrc.2019.01.103},
pmid = {30773255},
url = {https://doi.org/10.1016/j.bbrc.2019.01.103}
}
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Key findings
- The results displayed that the hyperphosphorylation of tau and NFs were increased in the STZ and Ex groups compared to the control and Dul groups.
- Dulaglutide also significantly shortened the escape latency and increased the number of hidden platform crossings in MWM test.
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Study details
- Evidence strengthLow
How this study scored 38/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multicenter collaboration, so those were left out: it earned 22 of the 58 points we could judge it on, which is 38 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Biochemical and biophysical research communications) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 2 / 5 | 2019 — within 10 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multicenter collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 30773255) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 22 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 22 of the 58 points we could judge it on is 38 out of 100. |
| Total | 38 / 100 | — |
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