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Psychosocial stress on neuroinflammation and cognitive dysfunctions in Alzheimer's disease: the emerging role for microglia?
Piirainen S, Youssef A, Song C, Kalueff AV, Landreth GE, Malm T, Tian L.. Neuroscience and biobehavioral reviews, 2017-02-06
Topic: Amyloid, tau and blood-test diagnosis
Chronic psychosocial stress is increasingly recognized as a risk factor for late-onset Alzheimer's disease (LOAD) and associated cognitive deficits. Chronic stress also primes microglia and induces inflammatory responses in the adult brain, thereby compromising synapse-supportive roles of microglia and deteriorating cognitive functions during aging. Substantial evidence demonstrates that failure of microglia to clear abnormally accumulating amyloid-beta (Aβ) peptide contributes to neuroinflammation and neurodegeneration in AD.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Piirainen, S., Youssef, A., Song, C., Kalueff, A. V., Landreth, G. E., Malm, T., et al. (2017). Psychosocial stress on neuroinflammation and cognitive dysfunctions in Alzheimer's disease: the emerging role for microglia? Neuroscience and biobehavioral reviews. https://doi.org/10.1016/j.neubiorev.2017.01.046
Vancouver
Piirainen S, Youssef A, Song C, Kalueff AV, Landreth GE, Malm T, et al. Psychosocial stress on neuroinflammation and cognitive dysfunctions in Alzheimer's disease: the emerging role for microglia? Neuroscience and biobehavioral reviews. 2017. doi:10.1016/j.neubiorev.2017.01.046. PMID: 28185874.
BibTeX
@article{piirainen2017-28185874,
author = {Piirainen, S. and Youssef, A. and Song, C. and Kalueff, A. V. and Landreth, G. E. and Malm, T. and Tian, L.},
title = {{Psychosocial stress on neuroinflammation and cognitive dysfunctions in Alzheimer's disease: the emerging role for microglia?}},
journal = {Neuroscience and biobehavioral reviews},
year = {2017},
doi = {10.1016/j.neubiorev.2017.01.046},
pmid = {28185874},
url = {https://doi.org/10.1016/j.neubiorev.2017.01.046}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
Key findings
- Chronic stress also primes microglia and induces inflammatory responses in the adult brain, thereby compromising synapse-supportive roles of microglia and deteriorating cognitive functions during aging.
- Substantial evidence demonstrates that failure of microglia to clear abnormally accumulating amyloid-beta (Aβ) peptide contributes to neuroinflammation and neurodegeneration in AD.
- Moreover, genome-wide association studies have linked variants in several immune genes, such as TREM2 and CD33, the expression of which in the brain is restricted to microglia, with cognitive dysfunctions in LOAD.
- Thus, inflammation-promoting chronic stress may create a vicious cycle of aggravated microglial dysfunction accompanied by increased Aβ accumulation, collectively exacerbating neurodegeneration.
Why it matters
This paper proposes that chronic psychosocial stress may raise the risk of late-onset Alzheimer's disease by priming microglia and triggering inflammation. It is a review of existing evidence, not a trial, so it does not show that reducing stress prevents or treats the disease.
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Study details
- Evidence strengthLow
How this study scored 45/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neuroscience and biobehavioral reviews) |
| Journal's citation record | 3 / 4 | Neuroscience & Biobehavioral Reviews: journal h-index 375 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 2 / 5 | 2017 — within 10 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 128 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 11.6 citations a year over 11 year(s) since 2017 |
| Impact for its field and year | 3 / 6 | Cited 7.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 2 other studies in this library |
| Still being cited | 2 / 4 | Cited 25 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Li Tian: h-index 41 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of Edinburgh: institution h-index 1,378 (OpenAlex) |
| Multi-centre collaboration | 3 / 3 | OpenAlex lists 13 institution(s) in 6 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 28185874) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 45 / 100 | — |
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