Evidence map›Paper›PMID 35228741›Full record

ReviewNature reviews. Neuroscience2022

Impaired insulin signalling and allostatic load in Alzheimer disease.

Fernanda G De Felice, Rafaella A Gonçalves, Sergio T Ferreira

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed, 2 pooled it
18.4field-weighted citation impact, top 1% 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

116 citing papers in PubMed, 2 syntheses or guidelines pooled it, 164 citations in OpenAlex.

  1. Pooled it
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  15. The landscape of dementia research, diagnosis, treatment, and care in Latin America.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
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  18. Estimated glucose disposal rate is associated with brain aging and dementia among diabetes-free older adults.The journals of gerontology. Series A, Biological sciences and medical sciences · 2026
    Article
  19. Review
  20. Article

56 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

3 authors at 2 institutions in 2 countries.

Fernanda G De FeliceCentre for Neuroscience Studies, Department of Biomedical and Molecular Sciences & Department of Psychiatry, Queen's University, Kingston, Ontario, Canada. fernanda.defelice@queensu.ca.
Rafaella A GonçalvesCentre for Neuroscience Studies, Department of Biomedical and Molecular Sciences & Department of Psychiatry, Queen's University, Kingston, Ontario, Canada.
Sergio T FerreiraInstitute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil.ORCID http://orcid.org/0000-0001-7160-9866
Queen's University · CAUniversidade Federal do Rio de Janeiro · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The discovery of insulin in 1921 revolutionized the treatment of diabetes and paved the way for numerous studies on hormone signalling networks and actions in peripheral tissues and in the central nervous system. Impaired insulin signalling, a hallmark of diabetes, is now established as a key component of Alzheimer disease (AD) pathology. Here, we review evidence showing that brain inflammation and activation of cellular stress response mechanisms comprise molecular underpinnings of impaired brain insulin signalling in AD and integrate impaired insulin signalling with AD pathology. Further, we highlight that insulin resistance is an important component of allostatic load and that allostatic overload can trigger insulin resistance. This bidirectional association between impaired insulin signalling and allostatic overload favours medical conditions that increase the risk of AD, including diabetes, obesity, depression, and cardiovascular and cerebrovascular diseases. Finally, we discuss how the integration of biological, social and lifestyle factors throughout the lifespan can contribute to the development of AD, underscoring the potential of social and lifestyle interventions to preserve brain health and prevent or delay AD.

Indexed as

AllostasisAlzheimer DiseaseInsulin ResistanceBrainHumansInsulinSignal TransductionInsulin

Identifiers

PMID35228741
OpenAlexW4214585512

What OpenQuestion holds

Textmetadata
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.