Evidence map›Paper›PMID 25237037›Full record

ReviewNeurobiology of disease2014

Insulin resistance in Alzheimer's disease.

Kelly T Dineley, Jordan B Jahrling, Larry Denner

Open access · greenAbstract readReview
In one paragraph

Review in Neurobiology of disease, 2014. 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
5.9field-weighted citation impact, top 3% 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, 122 citations in OpenAlex.

  1. Trial
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  14. Triglyceride Glucose Index is Related with the Risk of Mild Cognitive Impairment in Type 2 Diabetes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022
    Article
  15. The role of SLC transporters for brain health and disease.Cellular and molecular life sciences : CMLS · 2021
    Review
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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

3 authors at 1 institution in 1 country.

Kelly T DineleyDepartment of Neurology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Jordan B JahrlingDepartment of Neurology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Larry DennerDepartment of Internal Medicine, University of Texas Medical Branch, Galveston, TX 77555, USA. Electronic address: ladenner@utmb.edu.
The University of Texas Medical Branch at Galveston · US

Funding

Mechanisms of PPAR-gamma Enhancement of Cognitive Function in Alzheimer's DiseaseR01AG031859 · NIA · UNIVERSITY OF TEXAS MED BR GALVESTON · PI DENNER, LARRY, DINELEY, KELLY T · 2009 to 2013
$1.6M
NIA NIH HHS R01 AG031859NIA NIH HHS R01-AG031859
6 · The paper itself

Abstract

Insulin is a key hormone regulating metabolism. Insulin binding to cell surface insulin receptors engages many signaling intermediates operating in parallel and in series to control glucose, energy, and lipids while also regulating mitogenesis and development. Perturbations in the function of any of these intermediates, which occur in a variety of diseases, cause reduced sensitivity to insulin and insulin resistance with consequent metabolic dysfunction. Chronic inflammation ensues which exacerbates compromised metabolic homeostasis. Since insulin has a key role in learning and memory as well as directly regulating ERK, a kinase required for the type of learning and memory compromised in early Alzheimer's disease (AD), insulin resistance has been identified as a major risk factor for the onset of AD. Animal models of AD or insulin resistance or both demonstrate that AD pathology and impaired insulin signaling form a reciprocal relationship. Of note are human and animal model studies geared toward improving insulin resistance that have led to the identification of the nuclear receptor and transcription factor, peroxisome proliferator-activated receptor gamma (PPARγ) as an intervention tool for early AD. Strategic targeting of alternate nodes within the insulin signaling network has revealed disease-stage therapeutic windows in animal models that coalesce with previous and ongoing clinical trial approaches. Thus, exploiting the connection between insulin resistance and AD provides powerful opportunities to delineate therapeutic interventions that slow or block the pathogenesis of AD.

Indexed as

Insulin ResistanceAlzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainDisease Models, AnimalEncephalitisHumansInsulinLearningMAP Kinase Signaling SystemPPAR gammaAmyloid beta-PeptidesInsulinPPAR gammaAlzheimer's diseaseAnimal modelsCognitive functionERKInsulin resistanceLearning and memoryMetabolismMitochondriaPPAR gammaTherapeutic windows

Identifiers

PMID25237037
PMCPMC4253975
OpenAlexW1982390440

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.