Evidence map›Paper›PMID 29424027›Full record

ReviewNeuropathology and applied neurobiology2018

Review: Relationship of type 2 diabetes to human brain pathology.

J J Pruzin, P T Nelson, E L Abner, Z Arvanitakis

Abstract readReview
In one paragraph

Review in Neuropathology and applied neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
7.8field-weighted citation impact, top 2% of its field
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

51 citing papers in PubMed, 87 citations in OpenAlex.

  1. Diabetes-Associated Cognitive Impairment: Pathophysiology and Emerging Therapies.Annals of clinical and translational neurology · 2026
    Review
  2. Review
  3. Article
  4. QBP1 Peptide as a Potential Anti-Amyloidogenic Therapy for Type 2 Diabetes: An In Vitro Study.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Exploratory Dual PET imaging of [Bioorganic & medicinal chemistry letters · 2024
    Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
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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

4 authors at 2 institutions in 1 country.

J J PruzinRush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA.ORCID 0000-0001-7530-914X
P T NelsonSanders-Brown Center on Aging, University of Kentucky, Lexington, KY, USA.
E L AbnerSanders-Brown Center on Aging, University of Kentucky, Lexington, KY, USA.
Z ArvanitakisRush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA.
Rush University Medical Center · USUniversity of Kentucky · US

Funding

SUPPLEMENT TO RUSH ALZHEIMERS DISEASE CENTER COREP30AG010161 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 1991 to 2020
$49.1M
University of Kentucky Alzheimer's Disease Core Center - Biomarker CoreP30AG028383 · NIA · UNIVERSITY OF KENTUCKY · PI SCHMITT, FREDERICK · 2006 to 2020
$23.3M
Mechanisms linking insulin resistance to brain structure, pathology, and functionR01NS084965 · NINDS · RUSH UNIVERSITY MEDICAL CENTER · PI AHIMA, REXFORD S., ARNOLD, STEVEN E · 2014 to 2018
$3.2M
Vascular Cognitive and Motor Decline: Impact of aPLR01AG040039 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI ARVANITAKIS, ZOE · 2011 to 2015
$2.9M
NIA NIH HHS P30 AG010161NIA NIH HHS P30 AG028383NIA NIH HHS R01 AG040039NINDS NIH HHS R01 NS084965
6 · The paper itself

Abstract

Type 2 diabetes (T2D) and Alzheimer's disease (AD) are both highly prevalent diseases worldwide, and each is associated with high-morbidity and high-mortality. Numerous clinical studies have consistently shown that T2D confers a two-fold increased risk for a dementia, including dementia attributable to AD. Yet, the mechanisms underlying this relationship, especially nonvascular mechanisms, remain debated. Cerebral vascular disease (CVD) is likely to be playing a role. But increased AD neuropathologic changes (ADNC), specifically neuritic amyloid plaques (AP) and neurofibrillary tangles (NFT), are also posited mechanisms. The clinicopathological studies to date demonstrate T2D to be consistently associated with infarcts, particularly subcortical lacunar infarcts, but not ADNC, suggesting the association of T2D with dementia may largely be mediated through CVD. Furthermore, growing interest exists in insulin resistance (IR), particularly IR within the brain itself, which may be an associated but distinct phenomenon from T2D, and possibly itself associated with ADNC. Other mechanisms largely related to protein processing and efflux in the central nervous system with altered function in T2D may also be involved. Such mechanisms include islet amyloid polypeptide (or amylin) deposition, co-localized with beta-amyloid and found in more abundance in the AD temporal cortex, blood-brain barrier breakdown and dysfunction, potentially related to pericyte degeneration, and disturbance of brain lymphatics, both in the glial lymphatic system and the newly discovered discrete central nervous system lymph vessels. Medical research is ongoing to further disentangle the relationship of T2D to dementia in the ageing human brain.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesBrainDiabetes Mellitus, Type 2HumansNeurofibrillary TanglesPlaque, Amyloidtau ProteinsAmyloid beta-Peptidestau ProteinsAlzheimer's diseasecerebrovascular diseasediabetesinfarctioninsulin resistancepathology

Identifiers

PMID29424027
PMCPMC5980704
OpenAlexW2790084051

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.