Evidence map›Paper›PMID 28688899›Full record

ArticleNeurobiology of aging2017

Central insulin dysregulation and energy dyshomeostasis in two mouse models of Alzheimer's disease.

Ramon Velazquez, An Tran, Egide Ishimwe, Larry Denner, Nikhil Dave, Salvatore Oddo, Kelly T Dineley

Erratum issuedOpen access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurobiology of aging, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
6.4field-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

61 citing papers in PubMed, 97 citations in OpenAlex.

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1 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Ramon VelazquezArizona State University-Banner Neurodegenerative Disease Research Center at the Biodesign Institute, Arizona State University, Tempe, AZ, USA.
An TranArizona State University-Banner Neurodegenerative Disease Research Center at the Biodesign Institute, Arizona State University, Tempe, AZ, USA.
Egide IshimweDepartment of Neurology, Mitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch at Galveston (UTMB), Galveston, TX, USA.
Larry DennerInternal Medicine, Mitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch at Galveston (UTMB), Galveston, TX, USA.
Nikhil DaveArizona State University-Banner Neurodegenerative Disease Research Center at the Biodesign Institute, Arizona State University, Tempe, AZ, USA.
Salvatore OddoArizona State University-Banner Neurodegenerative Disease Research Center at the Biodesign Institute, Arizona State University, Tempe, AZ, USA; School of Life Sciences, Arizona State University, Tempe, AZ, USA. Electronic address: oddo@asu.edu.
Kelly T DineleyDepartment of Neurology, Mitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch at Galveston (UTMB), Galveston, TX, USA. Electronic address: ktdinele@utmb.edu.
Arizona State University · USThe 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
Molecular interplay between Abeta, tau and mTOR: Mechanisms of neurodegenerationR01AG037637 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI ODDO, SALVATORE · 2011 to 2015
$1.6M
Molecular interplay between Aβ, tau and mTOR: Mechanisms of neurodegenerationRF1AG037637 · NIA · ARIZONA STATE UNIVERSITY-TEMPE CAMPUS · PI ODDO, SALVATORE · 2016 to 2016
$1.1M
NIA NIH HHS R01 AG031859NIA NIH HHS R01 AG037637NIA NIH HHS RF1 AG037637
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder worldwide. While the causes of AD are not known, several risk factors have been identified. Among these, type two diabetes (T2D), a chronic metabolic disease, is one of the most prevalent risk factors for AD. Insulin resistance, which is associated with T2D, is defined as diminished or absent insulin signaling and is reflected by peripheral blood hyperglycemia and impaired glucose clearance. In this study, we used complementary approaches to probe for peripheral insulin resistance, central nervous system (CNS) insulin sensitivity and energy homeostasis in Tg2576 and 3xTg-AD mice, two widely used animal models of AD. We report that CNS insulin signaling abnormalities are evident months before peripheral insulin resistance. In addition, we find that brain energy metabolism is differentially altered in both mouse models, with 3xTg-AD mice showing more extensive changes. Collectively, our data suggest that early AD may reflect engagement of different signaling networks that influence CNS metabolism, which in turn may alter peripheral insulin signaling.

Indexed as

Insulin ResistanceAgingAlzheimer DiseaseAnimalsCentral Nervous SystemDiabetes Mellitus, Type 2Disease Models, AnimalEnergy MetabolismFemaleGlucoseHomeostasisHyperglycemiaInsulinMaleMice, TransgenicRisk FactorsGlucoseInsulin3xTg-ADAgingAlzheimer's diseaseEnergy metabolismGlucose tolerance testInsulin resistanceNeurodegenerationTg2576Type two diabetes

Identifiers

PMID28688899
PMCPMC5819888
OpenAlexW2651360079

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.