Evidence map›Paper›PMID 30106209›Full record

ReviewBrain pathology (Zurich, Switzerland)2019

Alzheimer's disease and type 2 diabetes mellitus are distinct diseases with potential overlapping metabolic dysfunction upstream of observed cognitive decline.

Yevgen Chornenkyy, Wang-Xia Wang, Angela Wei, Peter T Nelson

Open access · bronzeAbstract readReview
In one paragraph

Review in Brain pathology (Zurich, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 2 pooled it
8.5field-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

88 citing papers in PubMed, 2 syntheses or guidelines pooled it, 172 citations in OpenAlex.

  1. Pooled it
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  3. Neurovascular Actions of Dipeptidyl Peptidase-4 Inhibitors and Their Implications for Cognitive Dysfunction in Type 2 Diabetes Mellitus.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2026
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28 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Yevgen ChornenkyyUniversity of Kentucky College of Medicine, Lexington, KY.
Wang-Xia WangUniversity of Kentucky College of Medicine, Lexington, KY.
Angela WeiDepartment of Biology, University of Kentucky, Lexington, KY.
Peter T NelsonUniversity of Kentucky College of Medicine, Lexington, KY.ORCID 0000-0002-6161-1265
University of Kentucky · US

Funding

University of Kentucky Alzheimer's Disease Core Center - Biomarker CoreP30AG028383 · NIA · UNIVERSITY OF KENTUCKY · PI SCHMITT, FREDERICK · 2006 to 2020
$23.3M
Modulation of microRNA pathways by gemfibrozil in predementia Alzheimer diseaseR01AG042419 · NIA · UNIVERSITY OF KENTUCKY · PI JICHA, GREGORY A, NELSON, PETER T. · 2013 to 2016
$1.6M
CELLULAR CHANGES ALTERING SYNAPTIC CONNECTIVITY IN PRECLINICAL ADR01AG042475 · NIA · UNIVERSITY OF KENTUCKY · PI NELSON, PETER T. · 2013 to 2017
$1.5M
NIA NIH HHS P30 AG028383NIA NIH HHS R01 AG042419NIA NIH HHS R01 AG042475
6 · The paper itself

Abstract

Alzheimer's disease (AD) and type 2 diabetes mellitus (T2DM) are highly prevalent aging-related diseases associated with significant morbidity and mortality. Some findings in human and animal models have linked T2DM to AD-type dementia. Despite epidemiological associations between the T2DM and cognitive impairment, the interrelational mechanisms are unclear. The preponderance of evidence in longitudinal studies with autopsy confirmation have indicated that vascular mechanisms, rather than classic AD-type pathologies, underlie the cognitive decline often seen in self-reported T2DM. T2DM is associated with cardiovascular and cerebrovascular disease (CVD), and is associated with increased risk of infarcts and small vessel disease in the brain and other organs. Neuropathological examinations of post-mortem brains demonstrated evidence of cerebrovascular disease and little to no correlation between T2DM and β-amyloid deposits or neurofibrillary tangles. Nevertheless, the mechanisms upstream of early AD-specific pathology remain obscure. In this regard, there may indeed be overlap between the pathologic mechanisms of T2DM/"metabolic syndrome," and AD. More specifically, cerebral insulin processing, glucose metabolism, mitochondrial function, and/or lipid metabolism could be altered in patients in early AD and directly influence symptomatology and/or neuropathology.

Indexed as

Alzheimer DiseaseAnimalsBrainCerebrovascular DisordersCognitive DysfunctionDiabetes Mellitus, Type 2GlucoseHumansMitochondriaRisk FactorsGlucoseepidemiologymitochondrianeuropathologypathogenesispreclinicalVCID

Identifiers

PMID30106209
PMCPMC6427919
OpenAlexW2885296758

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.