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Metformin Ameliorates Aβ Pathology by Insulin-Degrading Enzyme in a Transgenic Mouse Model of Alzheimer's Disease
Lu XY, Huang S, Chen QB, Zhang D, Li W, Ao R, Leung FC, Zhang Z et al.. Oxidative medicine and cellular longevity, 2020-04-19
Topic: Brain proteins, microglia and lab models
Plain-language summary
Alzheimer's disease (AD) is the most common neurodegenerative disease. The accumulation of amyloid beta (A β ) is the main pathology of AD. Metformin, a well-known antidiabetic drug, has been reported to have AD-protective effect. However, the mechanism is still unclear. In this study, we tried to figure out whether metformin could activate insulin-degrading enzyme (IDE) to ameliorate A β -induced pathology. Morris water maze and Y-maze results indicated that metformin could improve the learning and memory ability in APP swe /PS1 dE9 (APP/PS1) transgenic mice. 18 F-FDG PET-CT result showed that metformin could ameliorate the neural dysfunction in APP/PS1 transgenic mice. PCR analysis showed that metformin could effectively improve the mRNA expression level of nerve and synapse-related genes ( Syp , Ngf , and Bdnf ) in the brain. Metformin decreased oxidative stress (malondialdehyde and superoxide dismutase) and neuroinflammation (IL-1 β and IL-6) in APP/PS1 mice. In addition, metformin obviously reduced the A β level in the brain of APP/PS1 mice. Metformin did not affect the enzyme activities and mRNA expression levels of A β -related secretases ( ADAM10 , BACE1 , and PS1 ). Meanwhile, metformin also did not affect the mRNA expression levels of A β -related transporters ( LRP1 and RAGE ). Metformin increased the protein levels of p-AMPK and IDE in the brain of APP/PS1 mice, which might be the key mechanism of metformin on AD. In conclusion, the well-known antidiabetic drug, metformin, could be a promising drug for AD treatment.
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APA 7th
Lu, X. Y., Huang, S., Chen, Q. B., Zhang, D., Li, W., Ao, R., et al. (2020). Metformin Ameliorates Aβ Pathology by Insulin-Degrading Enzyme in a Transgenic Mouse Model of Alzheimer's Disease. Oxidative medicine and cellular longevity. https://doi.org/10.1155/2020/2315106
Vancouver
Lu XY, Huang S, Chen QB, Zhang D, Li W, Ao R, et al. Metformin Ameliorates Aβ Pathology by Insulin-Degrading Enzyme in a Transgenic Mouse Model of Alzheimer's Disease. Oxidative medicine and cellular longevity. 2020. doi:10.1155/2020/2315106. PMID: 32377293.
BibTeX
@article{lu2020-32377293,
author = {Lu, X. Y. and Huang, S. and Chen, Q. B. and Zhang, D. and Li, W. and Ao, R. and Leung, F. C. and Zhang, Z. and others},
title = {{Metformin Ameliorates Aβ Pathology by Insulin-Degrading Enzyme in a Transgenic Mouse Model of Alzheimer's Disease}},
journal = {Oxidative medicine and cellular longevity},
year = {2020},
doi = {10.1155/2020/2315106},
pmid = {32377293},
url = {https://doi.org/10.1155/2020/2315106}
}
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Key findings
- Morris water maze and Y-maze results indicated that metformin could improve the learning and memory ability in APP swe /PS1 dE9 (APP/PS1) transgenic mice. 18 F-FDG PET-CT result showed that metformin could ameliorate the neural dysfunction in APP/PS1 transgenic mice.
- PCR analysis showed that metformin could effectively improve the mRNA expression level of nerve and synapse-related genes ( Syp , Ngf , and Bdnf ) in the brain.
- In conclusion, the well-known antidiabetic drug, metformin, could be a promising drug for AD treatment.
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Study details
- Evidence strengthLow
How this study scored 41/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported 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 24 of the 58 points we could judge it on, which is 41 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Oxidative medicine and cellular longevity) |
| 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 | 2020 — 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 | Laboratory or animal study (title names “transgenic”) — scores zero |
| 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 32377293) |
| Free to read | 2 / 2 | Free to read |
| Points | 24 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 24 of the 58 points we could judge it on is 41 out of 100. |
| Total | 41 / 100 | — |
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