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This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Brain scans and imaging

Topic: Brain proteins, microglia and lab models

Type 2 diabetes mellitus (T2DM) is a risk factor for Alzheimer disease (AD). Populations at risk for AD show altered brain activity in the default mode network (DMN) before cognitive dysfunction. We evaluated this brain pattern in T2DM patients. We compared T2DM patients (n = 10, age = 56 ± 2.2 years, fasting plasma glucose [FPG] = 8.4 ± 1.3 mmol/L, HbA(1c) = 7.5 ± 0.54%) with nondiabetic age-matched control subjects (n = 11, age = 54 ± 1.8 years, FPG = 4.8 ± 0.2 mmol/L) using resting-state functional magnetic resonance imaging to evaluate functional connectivity strength among DMN regions. We also evaluated hippocampal volume, cognition, and insulin sensitivity by homeostasis model assessment of insulin resistance (HOMA-IR). Control subjects showed stronger correlations versus T2DM patients in the DMN between the seed (posterior cingulate) and bilateral middle temporal gyrus (β = 0.67 vs. 0.43), the right inferior and left medial frontal gyri (β = 0.75 vs. 0.54), and the left thalamus (β = 0.59 vs. 0.37), respectively, with no group differences in cognition or hippocampal size. In T2DM patients, HOMA-IR was inversely correlated with functional connectivity in the right inferior frontal gyrus and precuneus. T2DM patients showed reduced functional connectivity in the DMN compared with control subjects, which was associated with insulin resistance in selected brain regions, but there were no group effects of brain structure or cognition.

Key findings

Why it matters

In a small comparison of 10 people with type 2 diabetes and 11 controls, the diabetes group showed reduced resting-state functional connectivity in the default mode network, with no group differences in cognition or hippocampal size. The sample is very small, and the study does not show that treating diabetes prevents Alzheimer disease.

Study details

How this study scored 50/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record 3 of 4; Study design 0 of 12; Strength of evidence 1 of 5; Peer-review validation 10 of 10; How recent 1 of 5; Sample size 0 of 4; Effect reported 2 of 3; Studied in people 0 of 3; Randomised / blinded 0 of 2; Times cited 5 of 7; Citations per year 3 of 5; Impact for its field and year 4 of 6; Cited by studies here 2 of 6; Still being cited 2 of 4; Senior author's track record 1 of 4; Institution's track record 3 of 3; Multi-centre collaboration 2 of 3; Indexed in PubMed 2 of 2; Free to read 2 of 2. Total 50 of 100.50 of 100 points earned50 not earned

Published in a peer-reviewed journal. Scored zero for study design, sample size, studied in people and randomised / blinded because the record does not state it.

ComponentPointsWhy
Journal tier 7 / 10 Tier 3 — peer-reviewed journal (Diabetes)
Journal's citation record 3 / 4 Diabetes: journal h-index 447 (OpenAlex, 2026-10-29)
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 2012 — 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 2 / 3 Effect reported as a number, without an interval or test
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 5 / 7 Cited 242 times (OpenAlex, 2026-10-10)
Citations per year 3 / 5 15.1 citations a year over 16 year(s) since 2012
Impact for its field and year 4 / 6 Cited 10.6× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 2 / 6 Cited by 6 other studies in this library
Still being cited 2 / 4 Cited 17 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 1 / 4 Last-listed author Wouter S. Hoogenboom: h-index 17 (OpenAlex, whole career)
Institution's track record 3 / 3 Harvard University: institution h-index 3,235 (OpenAlex)
Multi-centre collaboration 2 / 3 OpenAlex lists 7 institution(s) in 1 country
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 22664957)
Free to read 2 / 2 Free to read
Total 50 / 100 —

What each of these 20 components measures, and what this score is not →

Read the original

Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).

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. The record names 8 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.

APA 7th

Musen, G., Jacobson, A. M., Bolo, N. R., Simonson, D. C., Shenton, M. E., McCartney, R. L., et al. (2012). Resting-state brain functional connectivity is altered in type 2 diabetes. Diabetes. https://doi.org/10.2337/db11-1669

Vancouver

Musen G, Jacobson AM, Bolo NR, Simonson DC, Shenton ME, McCartney RL, et al. Resting-state brain functional connectivity is altered in type 2 diabetes. Diabetes. 2012. doi:10.2337/db11-1669. PMID: 22664957.

BibTeX

@article{musen2012-22664957,
  author  = {Musen, G. and Jacobson, A. M. and Bolo, N. R. and Simonson, D. C. and Shenton, M. E. and McCartney, R. L. and Flores, V. L. and Hoogenboom, W. S.},
  title   = {{Resting-state brain functional connectivity is altered in type 2 diabetes}},
  journal = {Diabetes},
  year    = {2012},
  doi     = {10.2337/db11-1669},
  pmid    = {22664957},
  url     = {https://doi.org/10.2337/db11-1669}
}

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