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[Insulin resistance and cognitive function]
Sasaoka T, Wada T, Tsuneki H.. Nihon rinsho. Japanese journal of clinical medicine, 2014-04-01
Topic: Risk, prevention and care in population studies
Risk of Alzheimer disease is increased in patients with diabetes. Insulin resistance is identified as a pathogenic mechanism of impaired cognitive dysfunction. Amyloid beta oligomers cause impaired insulin signaling at IRS-1 via mechanisms of TNFalpha and JNK activation.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Sasaoka, T., Wada, T., & Tsuneki, H. (2014). [Insulin resistance and cognitive function]. Nihon rinsho. Japanese journal of clinical medicine.
Vancouver
Sasaoka T, Wada T, Tsuneki H. [Insulin resistance and cognitive function]. Nihon rinsho. Japanese journal of clinical medicine. 2014. PMID: 24796090.
BibTeX
@article{sasaoka2014-24796090,
author = {Sasaoka, T. and Wada, T. and Tsuneki, H.},
title = {{[Insulin resistance and cognitive function]}},
journal = {Nihon rinsho. Japanese journal of clinical medicine},
year = {2014},
pmid = {24796090}
}
Built from the record alzhub holds for this paper, not looked up. This record has no DOI, so the citation leaves it out. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
Key findings
- Insulin resistance is identified as a pathogenic mechanism of impaired cognitive dysfunction.
- Amyloid beta oligomers cause impaired insulin signaling at IRS-1 via mechanisms of TNFalpha and JNK activation.
- Attenuation of PI-3 kinase pathway is also involved in the hyper-phosphorylation of Tau.
- Impairment of orexin function is connected to the age related insulin resistance and shortening of life expectancy.
Why it matters
This paper identifies insulin resistance as a mechanism of impaired cognitive dysfunction and notes that risk of Alzheimer disease is increased in patients with diabetes. It describes how amyloid beta oligomers impair insulin signaling and how attenuation of the PI-3 kinase pathway is involved in tau hyperphosphorylation.
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Study details
- Evidence strengthLow
How this study scored 29/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it. We have no data on journal's citation record, impact for its field and year and institution's track record, so those were left out: it earned 25 of the 87 points we could judge it on, which is 29 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Nihon rinsho. Japanese journal of clinical medicine) |
| 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 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 2 / 7 | Cited 12 times (OpenAlex, 2026-10-10) |
| Citations per year | 0 / 5 | 0.9 citations a year over 14 year(s) since 2014 |
| 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 | 0 / 6 | No other study in this library cites it |
| Still being cited | 0 / 4 | Cited 2 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Hiroshi Tsuneki: h-index 38 (OpenAlex, whole career) |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | 0 / 3 | OpenAlex lists 0 institution(s) in 0 countries — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 24796090) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 25 / 87 | Scored on 17 of 20 parts. We have no data for the rest, so they are left out: 25 of the 87 points we could judge it on is 29 out of 100. |
| Total | 29 / 100 | — |
What each of these 20 components measures, and what this score is not →
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