Evidence map›Paper›PMID 29992181›Full record

ReviewNeurobiology of stress2018

Chronic stress as a risk factor for Alzheimer's disease: Roles of microglia-mediated synaptic remodeling, inflammation, and oxidative stress.

Kanchan Bisht, Kaushik Sharma, Marie-Ève Tremblay

Open access · goldAbstract readReview
In one paragraph

Review in Neurobiology of stress, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 164 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
164citing papers in PubMed, 3 pooled it
17.1field-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

164 citing papers in PubMed, 3 syntheses or guidelines pooled it, 362 citations in OpenAlex.

  1. Pooled it
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  4. Article
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  6. Article
  7. Article
  8. Review
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  10. Review
  11. Review
  12. A Review on the Pathophysiology of Alzheimer's Disease.Current protein & peptide science · 2026
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Modulatory Effects ofAntioxidants (Basel, Switzerland) · 2025
    Review
  20. Article

104 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 1 institution in 1 country.

Kanchan BishtAxe Neurosciences, CRCHU de Québec-Université Laval, Québec, QC, Canada.
Kaushik SharmaAxe Neurosciences, CRCHU de Québec-Université Laval, Québec, QC, Canada.
Marie-Ève TremblayAxe Neurosciences, CRCHU de Québec-Université Laval, Québec, QC, Canada.
Université Laval · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microglia are the predominant immune cells of the central nervous system (CNS) that exert key physiological roles required for maintaining CNS homeostasis, notably in response to chronic stress, as well as mediating synaptic plasticity, learning and memory. The repeated exposure to stress confers a higher risk of developing neurodegenerative diseases including sporadic Alzheimer's disease (AD). While microglia have been causally linked to amyloid beta (Aβ) accumulation, tau pathology, neurodegeneration, and synaptic loss in AD, they were also attributed beneficial roles, notably in the phagocytic elimination of Aβ. In this review, we discuss the interactions between chronic stress and AD pathology, overview the roles played by microglia in AD, especially focusing on chronic stress as an environmental risk factor modulating their function, and present recently-described microglial phenotypes associated with neuroprotection in AD. These microglial phenotypes observed under both chronic stress and AD pathology may provide novel opportunities for the development of better-targeted therapeutic interventions.

Indexed as

ABCA7, ATP-binding cassette transporter A7AD, Alzheimer's diseaseAlzheimer's diseaseAPOE, Apolipoprotein EAPP, amyloid precursor proteinAβ, Amyloid betaBDNF, brain derived neurotrophic factorCD11b, cluster of differentiation molecule 11BCD33, cluster of differentiation 33CNS, central nervous systemCR, complement receptorCRF, corticotropin releasing factorDAM, disease associated microgliaDAP12, DNAX-activation protein 12Dark microgliaFAD, Familial Alzheimer's diseaseFCRLS, Fc receptor-like S scavenger receptorGR, glucocorticoid receptorHPA axis, hypothalamic pituitary adrenocortical axisIBA1, ionized calcium-binding adapter molecule 1IL, interleukinLTP, long-term potentiationMGnD, microglia with a neurodegenerative phenotypeMicrogliaMicroglial phenotypesmPFC, medial prefrontal cortexMR, mineralocorticoid receptorNADPH, nicotinamide adenine dinucleotide phosphateNeurodegenerationNeuroinflammationNFT, neurofibrillary tanglesPS, presenilinROS, reactive oxygen speciesStressSynaptic remodelingTGFβ, transforming growth factor βTLR, Toll-like receptorsTMEM119, transmembrane protein 119TNFα, tumor necrosis factor-αTREM2, triggering receptor expressed in myeloid cells 2TYROBP, TYRO protein tyrosine kinase binding protein

Identifiers

PMID29992181
PMCPMC6035903
OpenAlexW2804845995

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.