Home › Research › Drug development
Glucagon-like peptide-1 protects synaptic and learning functions from neuroinflammation in rodents
Takashi Iwai, Toshihiro Sawabe, Kahori Tanimitsu, Manabu Suzuki, Sachie Sasaki-Hamada, Jun-Ichiro Oka. Journal of neuroscience research, 2014-01-27
Topic: Gut, metabolism and diet
Glucagon-like peptide-1 (GLP-1) is derived from the processing of proglucagon in intestinal L-cells and releases insulin from pancreatic β-cells as an incretin. The GLP-1 receptor has been proposed as a possible therapeutic target for the treatment of Alzheimer's disease, in which neuroinflammation is critical in the pathogenesis. The present study investigates whether GLP-1 (7-36) amide, an active fragment of GLP-1, protected against synaptic impairments induced by inflammation-related injurious agents (lipopolysaccharide [LPS], interleukin-1β [IL-1β], and H2 O2). In the Y-maze test, LPS (10 μg/mouse, i.c.v) significantly decreased the percentage alternation. Pretreatment with GLP-1 (7-36) amide (0.09-0.9 nmol/mouse, i.c.v.) prevented an impairment in spontaneous alternation performance. Pretreatment with LPS (10 μg/ml, 2 hr) impaired LTP induction but not paired-pulse facilitation in the CA1 region of rat hippocampal slices. This impairment was prevented by cotreatment with GLP-1 (7-36) amide (50 nM). IL-1β (0.57 nM) or H2 O2 (50 μM) also impaired LTP induction. This impairment was prevented by GLP-1 (7-36) amide (50 nM). These results suggest that GLP-1 (7-36) amide improves the synaptic impairments induced by inflammation-related injurious agents in the CA1 region of the hippocampus.
Key findings
- In the Y-maze test, LPS (10 μg/mouse, i.c.v) significantly decreased the percentage alternation.
- These results suggest that GLP-1 (7-36) amide improves the synaptic impairments induced by inflammation-related injurious agents in the CA1 region of the hippocampus.
New to this subject? Start with our plain-English guide: Treatments →
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 and randomised / 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, multi-centre collaboration and free to read, so those were left out: it earned 21 of the 56 points we could judge it on, which is 38 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Journal of neuroscience research) |
| 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 | 1 / 5 | 2014 — within 20 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 | Laboratory or animal study (title names “rodents”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation 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 |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 24464856) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 21 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 21 of the 56 points we could judge it on is 38 out of 100. |
| Total | 38 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
Free copy unknown: no free-copy check has an answer for this record yet. That does not mean it is paywalled.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
APA 7th
Iwai, T., Sawabe, T., Tanimitsu, K., Suzuki, M., Sasaki-Hamada, S., & Oka, J.-I. (2014). Glucagon-like peptide-1 protects synaptic and learning functions from neuroinflammation in rodents. Journal of neuroscience research. https://doi.org/10.1002/jnr.23335
Vancouver
Iwai T, Sawabe T, Tanimitsu K, Suzuki M, Sasaki-Hamada S, Oka J.-I. Glucagon-like peptide-1 protects synaptic and learning functions from neuroinflammation in rodents. Journal of neuroscience research. 2014. doi:10.1002/jnr.23335. PMID: 24464856.
BibTeX
@article{iwai2014-24464856,
author = {Iwai, Takashi and Sawabe, Toshihiro and Tanimitsu, Kahori and Suzuki, Manabu and Sasaki-Hamada, Sachie and Oka, Jun-Ichiro},
title = {{Glucagon-like peptide-1 protects synaptic and learning functions from neuroinflammation in rodents}},
journal = {Journal of neuroscience research},
year = {2014},
doi = {10.1002/jnr.23335},
pmid = {24464856},
url = {https://doi.org/10.1002/jnr.23335}
}