Evidence map›Paper›PMID 29888312›Full record

ReviewNeurobiology of stress2018

A preclinical perspective on the enhanced vulnerability to Alzheimer's disease after early-life stress.

Lianne Hoeijmakers, Sylvie L Lesuis, Harm Krugers, Paul J Lucassen, Aniko Korosi

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 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
  2. Stress, stress systems, and Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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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

5 authors at 1 institution in 1 country.

Lianne HoeijmakersBrain Plasticity Group, Center for Neuroscience, Swammerdam Institute for Life Sciences, University of Amsterdam, Science Park 904, Amsterdam, The Netherlands.
Sylvie L LesuisBrain Plasticity Group, Center for Neuroscience, Swammerdam Institute for Life Sciences, University of Amsterdam, Science Park 904, Amsterdam, The Netherlands.
Harm KrugersBrain Plasticity Group, Center for Neuroscience, Swammerdam Institute for Life Sciences, University of Amsterdam, Science Park 904, Amsterdam, The Netherlands.
Paul J LucassenBrain Plasticity Group, Center for Neuroscience, Swammerdam Institute for Life Sciences, University of Amsterdam, Science Park 904, Amsterdam, The Netherlands.
Aniko KorosiBrain Plasticity Group, Center for Neuroscience, Swammerdam Institute for Life Sciences, University of Amsterdam, Science Park 904, Amsterdam, The Netherlands.
Netherlands Institute for Neuroscience · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stress experienced early in life (ES), in the form of childhood maltreatment, maternal neglect or trauma, enhances the risk for cognitive decline in later life. Several epidemiological studies have now shown that environmental and adult life style factors influence AD incidence or age-of-onset and early-life environmental conditions have attracted attention in this respect. There is now emerging interest in understanding whether ES impacts the risk to develop age-related neurodegenerative disorders, and their severity, such as in Alzheimer's disease (AD), which is characterized by cognitive decline and extensive (hippocampal) neuropathology. While this might be relevant for the identification of individuals at risk and preventive strategies, this topic and its possible underlying mechanisms have been poorly studied to date. In this review, we discuss the role of ES in modulating AD risk and progression, primarily from a preclinical perspective. We focus on the possible involvement of stress-related, neuro-inflammatory and metabolic factors in mediating ES-induced effects on later neuropathology and the associated impairments in neuroplasticity. The available studies suggest that the age of onset and progression of AD-related neuropathology and cognitive decline can be affected by ES, and may aggravate the progression of AD neuropathology. These relevant changes in AD pathology after ES exposure in animal models call for future clinical studies to elucidate whether stress exposure during the early-life period in humans modulates later vulnerability for AD.

Identifiers

PMID29888312
PMCPMC5991337
OpenAlexW2791785701

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.