Evidence map›Paper›PMID 29163128›Full record

ReviewFrontiers in aging neuroscience2017

Insulin Resistance and Alzheimer's Disease: Bioenergetic Linkages.

Bryan J Neth, Suzanne Craft

Abstract readReview
In one paragraph

Review in Frontiers in aging neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 160 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
160citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

160 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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100 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

2 authors.

Bryan J NethDepartment of Internal Medicine, Section on Gerontology and Geriatric Medicine, Wake Forest School of Medicine, Winston-Salem, NC, United States.
Suzanne CraftDepartment of Internal Medicine, Section on Gerontology and Geriatric Medicine, Wake Forest School of Medicine, Winston-Salem, NC, United States.

Funding

Wake Forest Alzheimer's Disease Core CenterP30AG049638 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI WILLIAMSON, JEFF DOUGLAS · 2016 to 2020
$12.2M
Glucose Regulation and Memory in Alzheimer's DiseaseR37AG010880 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CRAFT, SUZANNE · 2005 to 2014
$5.2M
Therapeutic Effects of Intranasal Insulin in ADR01AG027415 · NIA · UNIVERSITY OF WASHINGTON · PI CRAFT, SUZANNE · 2006 to 2008
$1.2M
NIA NIH HHS P30 AG049638NIA NIH HHS R01 AG027415NIA NIH HHS R37 AG010880
6 · The paper itself

Abstract

Metabolic dysfunction is a well-established feature of Alzheimer's disease (AD), evidenced by brain glucose hypometabolism that can be observed potentially decades prior to the development of AD symptoms. Furthermore, there is mounting support for an association between metabolic disease and the development of AD and related dementias. Individuals with insulin resistance, type 2 diabetes mellitus (T2D), hyperlipidemia, obesity, or other metabolic disease may have increased risk for the development of AD and similar conditions, such as vascular dementia. This association may in part be due to the systemic mitochondrial dysfunction that is common to these pathologies. Accumulating evidence suggests that mitochondrial dysfunction is a significant feature of AD and may play a fundamental role in its pathogenesis. In fact, aging itself presents a unique challenge due to inherent mitochondrial dysfunction and prevalence of chronic metabolic disease. Despite the progress made in understanding the pathogenesis of AD and in the development of potential therapies, at present we remain without a disease-modifying treatment. In this review, we will discuss insulin resistance as a contributing factor to the pathogenesis of AD, as well as the metabolic and bioenergetic disruptions linking insulin resistance and AD. We will also focus on potential neuroimaging tools for the study of the metabolic dysfunction commonly seen in AD with hopes of developing therapeutic and preventative targets.

Indexed as

Alzheimer’s diseasebioenergetic shiftinflammationinsulin resistanceketone bodymetabolismpositron emission tomography

Identifiers

PMID29163128
PMCPMC5671587

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.