Evidence map›Paper›PMID 21320489›Full record

ReviewExperimental neurology2012

Diabetes as a chronic metabolic stressor: causes, consequences and clinical complications.

Lawrence P Reagan

Registry-linked trialAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Experimental neurology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03580967 (Vortioxetine Monotherapy for Major Depressive Disorder in Type 2 Diabetes), which is not on this map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.7field-weighted citation impact, top 5% 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.

NCT03580967 phase4withdrawnnot on this mapstarted 2019, after this paper: background citation

Vortioxetine Monotherapy for Major Depressive Disorder in Type 2 Diabetes: Role of Inflammation, Kynurenine Pathway, and Structural and Functional Brain Connectivity as Biomarkers

TypeinterventionalSponsorTodd DoyleRan2019 to 2021Enrolled0ConditionsType2 Diabetes, Major Depressive DisorderArmsVortioxetine
3 · Its place in the literature

Who cites it

43 citing papers in PubMed, 97 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Pursuing the Molecular Nexus Connecting Diabetes and the Associated Cognitive Impairments.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review
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

1 author at 1 institution in 1 country.

Lawrence P ReaganDepartment of Pharmacology, Physiology & Neuroscience, University of South Carolina School of Medicine, Columbia, SC 29208, USA. lpreagan@uscmed.sc.edu
University of South Carolina · US

Funding

INSULIN AND CNS CONTROL OF BODY WEIGHT AND FOOD INTAKER01DK017844 · NIDDK · UNIVERSITY OF WASHINGTON · PI WOODS, STEPHEN C · 1986 to 2013
$3.8M
Hippocampal insulin signaling deficits in diabetic ratsR01NS047728 · NINDS · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI REAGAN, LAWRENCE P · 2005 to 2008
$1.2M
INSULIN AND CNS CONTROL OF BODY WEIGHT AND FOOD INTAKER37DK017844 · NIDDK · UNIVERSITY OF WASHINGTON · PI WOODS, STEPHEN C · 1993 to 2000
$382k
Hippocampal plasticity in co-morbid diabetes and depressionR21MH086067 · NIMH · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI MOTT, DAVID D, REAGAN, LAWRENCE P · 2009 to 2010
$355k
NIDDK NIH HHS DK017844NIDDK NIH HHS R01 DK017844NIDDK NIH HHS R37 DK017844NIMH NIH HHS MH086067NIMH NIH HHS R21 MH086067NINDS NIH HHS NS047728NINDS NIH HHS R01 NS047728
6 · The paper itself

Abstract

Diabetes mellitus is an endocrine disorder resulting from inadequate insulin release and/or reduced insulin sensitivity. The complications of diabetes are well characterized in peripheral tissues, but there is a growing appreciation that the complications of diabetes extend to the central nervous system (CNS). One of the potential neurological complications of diabetes is cognitive deficits. Interestingly, the structural, electrophysiological, neurochemical and anatomical underpinnings responsible for cognitive deficits in diabetes are strikingly similar to those observed in animals subjected to chronic stress, as well as in patients with stress-related psychiatric illnesses such as major depressive disorder. Since diabetes is a chronic metabolic stressor, this has led to the suggestion that common mechanistic mediators are responsible for neuroplasticity deficits in both diabetes and depression. Moreover, these common mechanistic mediators may be responsible for the increase in the risk of depressive illness in diabetes patients. In view of these observations, the aims of this review are (1) to describe the neuroplasticity deficits observed in diabetic rodents and patients; (2) to summarize the similarities in the clinical and preclinical studies of depression and diabetes; and (3) to highlight the diabetes-induced neuroplasticity deficits in those brain regions that have been implicated as important pathological centers in depressive illness, namely, the hippocampus, the amygdala and the prefrontal cortex.

Indexed as

AnimalsBrainCognition DisordersDiabetes MellitusDisease Models, AnimalHumansNeuronal PlasticityStress, Psychological

Identifiers

PMID21320489
PMCPMC3110581
OpenAlexW2152771413

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.