Evidence map›Paper›PMID 42151730›Full record

ReviewAlzheimer's & dementia : the journal of the Alzheimer's Association2026

How does type 2 diabetes modify the risk of Alzheimer's disease?

G T Sutherland, A Chen, H-T Nguyen-Hao, H Mundell, E Aladyeva, M J Hofer, O Harari, S M Twigg

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

G T SutherlandSydney Brainomics, School of Medical Sciences and Charles Perkins Centre Faculty of Medicine and Health, The University of Sydney, Camperdown, New South Wales, Australia.ORCID https://orcid.org/0000-0003-2493-9736
A ChenSydney Brainomics, School of Medical Sciences and Charles Perkins Centre Faculty of Medicine and Health, The University of Sydney, Camperdown, New South Wales, Australia.
H-T Nguyen-HaoSydney Brainomics, School of Medical Sciences and Charles Perkins Centre Faculty of Medicine and Health, The University of Sydney, Camperdown, New South Wales, Australia.
H MundellSydney Brainomics, School of Medical Sciences and Charles Perkins Centre Faculty of Medicine and Health, The University of Sydney, Camperdown, New South Wales, Australia.
E AladyevaDepartment of Neurology and Neurological Research Institute, Ohio State University, Columbus, Ohio, USA.
M J HoferSchool of Life and Environmental Sciences and Charles Perkins Centre, Faculty of Science, The University of Sydney, Sydney, New South Wales, Australia.
O HarariDepartment of Neurology and Neurological Research Institute, Ohio State University, Columbus, Ohio, USA.
S M TwiggGreg Brown Diabetes & Endocrine Research Laboratory, Charles Perkins Centre, Charles Perkins Centre, The University of Sydney, Camperdown, New South Wales, Australia.

Funding

Lucas Papaw Foundation
6 · The paper itself

Abstract

Type 2 diabetes (T2D) and Alzheimer's disease (AD) are both increasing exponentially worldwide. T2D has also been identified as one of 14 modifiable risk factors for dementia, but the mechanism is unknown. T2D could promote dementia via vascular or AD neuropathological changes, and mechanistic hypotheses include central insulin resistance and T2D's peripheral inflammation promoting central inflammation. Here we examine these different hypotheses by reviewing the recent literature in combination with re-analysis of post mortem brain tissue molecular data. Collectively, recent studies and single-cell transcriptomic data suggest that peripheral lipid anomalies and inflammation seen in T2D act together to reduce brain-blood barrier integrity, facilitating aberrant immune signaling between the periphery and the brain. The subsequent promotion of AD-specific microglial subtypes is the most likely mechanism linking T2D and AD. These AD-specific microglial subtypes may be reduced by therapeutic targeting of triggering receptor expressed on myeloid cells 2-apolipoprotein E signaling pathway.

Indexed as

Alzheimer DiseaseDiabetes Mellitus, Type 2AnimalsBrainHumansInflammationMicrogliaRisk FactorsAlzheimer's diseaseglucoselipidsmicrogliatranscriptomicsType 2 diabetes

Identifiers

PMID42151730
PMCPMC13183603

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.