Evidence map›Paper›PMID 35970828›Full record

ReviewCell death & disease2022

ER stress and UPR in Alzheimer's disease: mechanisms, pathogenesis, treatments.

Amir Ajoolabady, Dan Lindholm, Jun Ren, Domenico Pratico

Open access · goldAbstract readReview
In one paragraph

Review in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
149citing papers in PubMed, 1 pooled it
23.3field-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

149 citing papers in PubMed, 1 synthesis or guideline pooled it, 214 citations in OpenAlex.

  1. Pooled it
  2. Article
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  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Identification of chemicals targeting dementia genes and pathways in the Comparative Toxicogenomics Database.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  11. SIEVEseq: unified differential expression, variability, and skewness analyses using RNA-Seq data.DNA research : an international journal for rapid publication of reports on genes and genomes · 2026
    Article
  12. Beneficially Stressing the Peripheral Nervous System to Repair.International journal of molecular sciences · 2026
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Neuroinflammation and Tauopathies.Molecular biology reports · 2026
    Review
  18. Article
  19. Article
  20. Article

89 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

4 authors at 4 institutions in 3 countries.

Amir AjoolabadyShanghai Institute of Cardiovascular Diseases, Department of Cardiology, Zhongshan Hospital Fudan University, Shanghai, China.
Dan LindholmMinerva Foundation Institute for Medical Research, Helsinki, Finland.
Jun RenShanghai Institute of Cardiovascular Diseases, Department of Cardiology, Zhongshan Hospital Fudan University, Shanghai, China. jren@uw.edu.
Domenico PraticoAlzheimer's Center at Temple, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA. praticod@temple.edu.ORCID 0000-0002-8347-613X
Fudan University · CNTemple University · USUniversity of Helsinki · FIUniversity of Washington · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a devastating neurodegenerative disorder characterized by gradual loss of memory and cognitive function, which constitutes a heavy burden on the healthcare system globally. Current therapeutics to interfere with the underlying disease process in AD is still under development. Although many efforts have centered on the toxic forms of Aβ to effectively tackle AD, considering the unsatisfactory results so far it is vital to examine other targets and therapeutic approaches as well. The endoplasmic reticulum (ER) stress refers to the build-up of unfolded or misfolded proteins within the ER, thus, perturbing the ER and cellular homeostasis. Emerging evidence indicates that ER stress contributes to the onset and development of AD. A thorough elucidation of ER stress machinery in AD pathology may help to open up new therapeutic avenues in the management of this devastating condition to relieve the cognitive dementia symptoms. Herein, we aim at deciphering the unique role of ER stress in AD pathogenesis, reviewing key findings, and existing controversy in an attempt to summarize plausible therapeutic interventions in the management of AD pathophysiology.

Indexed as

Alzheimer DiseaseEndoplasmic Reticulum StressHumansUnfolded Protein Response

Identifiers

PMID35970828
PMCPMC9378716
OpenAlexW4291464609

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.