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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 68 out of 100. Risk factors

Topic: Amyloid, tau and blood-test diagnosis

We performed a systematic review and meta-analysis to explore whether type 2 diabetes mellitus (T2DM) increases the risk of Alzheimer's disease (AD). We also reviewed interactions with smoking, hypertension, and apolipoprotein E ɛ4. Using a series of databases (MEDLINE, EMBASE, PubMed, Current Contents Connect, and Google Scholar), we identified a total of 15 epidemiologic studies. Fourteen studies reported positive associations, of which 9 were statistically significant. Risk estimates ranged from 0.83 to 2.45. The pooled adjusted risk ratio was 1.57 (95% confidence interval: 1.41, 1.75), with a population-attributable risk of 8%. Smoking and hypertension, when comorbid with T2DM, had odds of 14 and 3, respectively. Of the 5 studies that investigated the interaction between T2DM and apolipoprotein E ɛ4, 4 showed positive associations, of which 3 were significant, with odds ranging from 2.4 to 4.99. The pooled adjusted risk ratio was 2.91 (95% confidence interval: 1.51, 5.61). Risk estimates were presented in the context of a key confounder-cerebral infarcts-which are more common in those with T2DM and might contribute to the manifestation of clinical AD. We provide evidence from clinico-neuropathologic studies that demonstrates the following: First, cerebral infarcts are more common than AD-type pathology in those with T2DM and dementia. Second, those with dementia at postmortem are more likely to have both AD-type and cerebrovascular pathologies. Finally, cerebral infarcts reduce the number of AD lesions required for the manifestation of clinical dementia, but they do not appear to interact synergistically with AD-type pathology. Therefore, the increased risk of clinically diagnosed AD seems to be mediated through cerebrovascular pathology.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Vagelatos, N. T., & Eslick, G. D. (2013). Type 2 diabetes as a risk factor for Alzheimer's disease: the confounders, interactions, and neuropathology associated with this relationship. Epidemiologic reviews. https://doi.org/10.1093/epirev/mxs012

Vancouver

Vagelatos NT, Eslick GD. Type 2 diabetes as a risk factor for Alzheimer's disease: the confounders, interactions, and neuropathology associated with this relationship. Epidemiologic reviews. 2013. doi:10.1093/epirev/mxs012. PMID: 23314404.

BibTeX

@article{vagelatos2013-23314404,
  author  = {Vagelatos, N. T. and Eslick, G. D.},
  title   = {{Type 2 diabetes as a risk factor for Alzheimer's disease: the confounders, interactions, and neuropathology associated with this relationship}},
  journal = {Epidemiologic reviews},
  year    = {2013},
  doi     = {10.1093/epirev/mxs012},
  pmid    = {23314404},
  url     = {https://doi.org/10.1093/epirev/mxs012}
}

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.

Key findings

Why it matters

This systematic review and meta-analysis found that type 2 diabetes was associated with an increased risk of Alzheimer's disease, with a pooled adjusted risk ratio of 1.57, and that the increased risk seemed to be mediated through cerebrovascular pathology such as cerebral infarcts. It identifies diabetes as a risk factor but does not show that treating diabetes prevents or cures Alzheimer's disease.

Study details

How this study scored 68/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record 2 of 4; Study design 12 of 12; Strength of evidence 5 of 5; Peer-review validation 10 of 10; How recent 1 of 5; Sample size 1 of 4; Effect reported 0 of 3; Studied in people 3 of 3; Randomised / blinded 0 of 2; Times cited 6 of 7; Citations per year 4 of 5; Impact for its field and year 4 of 6; Cited by studies here 3 of 6; Still being cited 3 of 4; Senior author's track record 3 of 4; Institution's track record 1 of 3; Multi-centre collaboration 1 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. Total 68 of 100.68 of 100 points earned32 not earned

Published in a peer-reviewed journal, and it is a systematic review of all the studies on the question. Scored zero for effect reported because the record does not state it.

ComponentPointsWhy
Journal tier 7 / 10 Tier 3 — peer-reviewed journal (Epidemiologic reviews)
Journal's citation record 2 / 4 Epidemiologic Reviews: journal h-index 178 (OpenAlex, 2026-10-29)
Study design 12 / 12 A systematic review of all the studies on the question
Strength of evidence 5 / 5 Rated “high” in our summary
Peer-review validation 10 / 10 Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent 1 / 5 2013 — within 20 year(s) of the newest study here
Sample size 1 / 4 15 participants
Effect reported 0 / 3 No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people 3 / 3 Studied in people (participant count stated)
Randomised / blinded 0 / 2 A review of other studies — randomisation is not credited here
Times cited 6 / 7 Cited 320 times (OpenAlex, 2026-10-10)
Citations per year 4 / 5 21.3 citations a year over 15 year(s) since 2013
Impact for its field and year 4 / 6 Cited 17.7× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 3 / 6 Cited by 24 other studies in this library
Still being cited 3 / 4 Cited 58 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 3 / 4 Last-listed author Guy D. Eslick: h-index 72 (OpenAlex, whole career)
Institution's track record 1 / 3 The University of Sydney: institution h-index 1,466 (OpenAlex)
Multi-centre collaboration 1 / 3 OpenAlex lists 2 institution(s) in 1 country
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 23314404)
Free to read 0 / 2 Behind a paywall — scores zero
Total 68 / 100 —

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

Read the original

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