Evidence map›Paper›PMID 27988872›Full record

ReviewDrugs2017

Insulin Resistance and Neurodegeneration: Progress Towards the Development of New Therapeutics for Alzheimer's Disease.

Suzanne M de la Monte

Abstract readReview
In one paragraph

Review in Drugs, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 179 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
179citing papers in PubMed, 4 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

179 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
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  17. Special Issue: "Molecular Diagnosis and Treatments of Diabetes Mellitus".International journal of molecular sciences · 2025
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119 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

1 author.

Suzanne M de la MonteDepartment of Neurology, Rhode Island Hospital, and the Alpert Medical School of Brown University, Pierre Galletti Research Building, 55 Claverick Street, Room 419, Providence, RI, 02903, USA. Suzanne_DeLaMonte_MD@Brown.edu.

Funding

FASD Inhibition of ASPH-Notch Mediates Adolescent Cerebral White Matter Pathology-Potential Utility of Non-invasive Extracellular Vesicle AssaysR01AA011431 · NIAAA · RHODE ISLAND HOSPITAL (PROVIDENCE, RI) · PI SUZANNE M. DE LA MONTE · 1996 to 2026
$5.4M
Ethanol, IRS-1 Signaling and Neuronal MigrationR37AA011431 · NIAAA · RHODE ISLAND HOSPITAL · PI DE LA MONTE, SUZANNE M. · 2009 to 2018
$3.7M
Clinical Evaluation of T3D-959 as a Potential Disease Remedial Therapeutic for the Treatment of Alzheimer's DiseaseR44AG049510 · NIA · T3D THERAPEUTICS, INC. · PI DE LA MONTE, SUZANNE M., DIDSBURY, JOHN · 2015 to 2016
$1.9M
ETHANOL, INSULIN/IGF SIGNALING AND NEURONAL MIGRATIONR56AA011431 · NIAAA · RHODE ISLAND HOSPITAL · PI DE LA MONTE, SUZANNE M. · 2008 to 2008
$312k
NIAAA NIH HHS R01 AA011431NIAAA NIH HHS R37 AA011431NIAAA NIH HHS R56 AA011431NIA NIH HHS R44 AG049510
6 · The paper itself

Abstract

Alzheimer's disease (AD) should be regarded as a degenerative metabolic disease caused by brain insulin resistance and deficiency, and overlapping with the molecular, biochemical, pathophysiological, and metabolic dysfunctions in diabetes mellitus, non-alcoholic fatty liver disease, and metabolic syndrome. Although most of the diagnostic and therapeutic approaches over the past several decades have focused on amyloid-beta (Aβ42) and aberrantly phosphorylated tau, which could be caused by consequences of brain insulin resistance, the broader array of pathologies including white matter atrophy with loss of myelinated fibrils and leukoaraiosis, non-Aβ42 microvascular disease, dysregulated lipid metabolism, mitochondrial dysfunction, astrocytic gliosis, neuro-inflammation, and loss of synapses vis-à-vis growth of dystrophic neurites, is not readily accounted for by Aβ42 accumulations, but could be explained by dysregulated insulin/IGF-1 signaling with attendant impairments in signal transduction and gene expression. This review covers the diverse range of brain abnormalities in AD and discusses how insulins, incretins, and insulin sensitizers could be utilized to treat at different stages of neurodegeneration.

Indexed as

Insulin ResistanceAlzheimer DiseaseHumansNeuroprotective AgentsNeuroprotective Agents

Identifiers

PMID27988872
PMCPMC5575843

What OpenQuestion holds

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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.