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38/100

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Treatments

Topic: Brain proteins, microglia and lab models

Plain-language summary

Rational Epidemiological evidence suggests that individuals with diabetes mellitus are at greater risk of developing Alzheimer's disease, and controversy overwhelms the usefulness of the widely prescribed insulin-sensitizing drug, metformin, on cognition. Objectives Through the scopolamine-induced memory deficit model, we investigated metformin influence on cognitive dysfunction and explored underlying mechanisms. Methods Sixty adult male Wistar rats were randomly assigned into 5 groups (12 rats each) to receive either normal saline, scopolamine 1 mg/kg intraperitoneally once daily, scopolamine + oral metformin (100 mg/kg/day), scopolamine + oral metformin (300 mg/kg/day) or scopolamine + oral rivastigmine (0.75 mg/kg/day) for 14 days. Cognitive behaviours were tested using Morris water maze and passive avoidance tasks. Biochemically, brain oxidative (malondialdehyde) and inflammatory (TNF-α) markers, nitric oxide, Akt, phospho-Akt, phospho-tau and acetyl cholinesterase activity in hippocampal and cortical tissues were assessed. Results The lower dose of metformin (100 mg/kg) ameliorated scopolamine-induced impaired performance in both Morris water maze and passive avoidance tasks, and was associated with significant reduction of inflammation and to a lesser extent oxidative stress versus rivastigmine. Given the role of total Akt in regulation of abnormal tau accumulation and degradation, our finding that metformin 100 decreased the elevated total Akt while increasing its phosphorylated form explains its beneficial modulatory effect on phosphorylated tau in both tissues, and could further clarify its protection against memory impairment. Conclusion Metformin, only in the average human antidiabetic dose, offers a protective effect against scopolamine-induced cognitive impairment, while no deleterious effect was observed with the higher dose, which may support a bonus effect of metformin in type 2 diabetic patients.

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APA 7th

Mostafa, D. K., Ismail, C. A., & Ghareeb, D. A. (2016). Differential metformin dose-dependent effects on cognition in rats: role of Akt. Psychopharmacology. https://doi.org/10.1007/s00213-016-4301-2

Vancouver

Mostafa DK, Ismail CA, Ghareeb DA. Differential metformin dose-dependent effects on cognition in rats: role of Akt. Psychopharmacology. 2016. doi:10.1007/s00213-016-4301-2. PMID: 27113224.

BibTeX

@article{mostafa2016-27113224,
  author  = {Mostafa, D. K. and Ismail, C. A. and Ghareeb, D. A.},
  title   = {{Differential metformin dose-dependent effects on cognition in rats: role of Akt}},
  journal = {Psychopharmacology},
  year    = {2016},
  doi     = {10.1007/s00213-016-4301-2},
  pmid    = {27113224},
  url     = {https://doi.org/10.1007/s00213-016-4301-2}
}

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Key findings

Rational Epidemiological evidence suggests that individuals with diabetes mellitus are at greater risk of developing Alzheimer's disease, and controversy overwhelms the usefulness of the widely prescribed insulin-sensitizing drug, metformin, on cognition.
Results The lower dose of metformin (100 mg/kg) ameliorated scopolamine-induced impaired performance in both Morris water maze and passive avoidance tasks, and was associated with significant reduction of inflammation and to a lesser extent oxidative stress versus rivastigmine.

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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 and effect reported 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 (Psychopharmacology)
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	2016 — 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 “rats”) — scores zero
Randomized / blinded	1 / 2	Randomized (as stated in the record)
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 27113224)
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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