Evidence map›Paper›PMID 24619348›Full record

ReviewNature reviews. Neuroscience2014

Disturbance of endoplasmic reticulum proteostasis in neurodegenerative diseases.

Claudio Hetz, Bertrand Mollereau

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 361 papers.

0numbers the graph read from it
0cells of the map it votes in
361citing papers in PubMed
–field-weighted citation impact
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

361 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. How Do Amyloid Pathology and Aberrant Neuronal Activity Disrupt Plasticity and Memory in Alzheimer's Disease?The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Alzheimer's disease risk geneBrain communications · 2026
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. A New GlyT2 Variant Associated with Hyperekplexia.International journal of molecular sciences · 2025
    Article
  20. Article

301 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

2 authors.

Claudio Hetz1] Biomedical Neuroscience Institute, Faculty of Medicine, University of Chile, Santiago, Chile. [2] Institute of Biomedical Sciences, Center for Molecular Studies of the Cell, Program of Cellular and Molecular Biology, University of Chile, Santiago, Chile. [3] Neurounion Biomedical Foundation, Santiago, Chile. [4] Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts 02115, USA.
Bertrand MollereauLaboratory of Molecular Biology of the Cell, CNRS UMR5239, Ecole Normale Supérieure de Lyon, UMS3444 Biosciences Lyon Gerland, University of Lyon, Lyon 69364, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The unfolded protein response (UPR) is a homeostatic mechanism by which cells regulate levels of misfolded proteins in the endoplasmic reticulum (ER). Although it is well characterized in non-neuronal cells, a proliferation of papers over the past few years has revealed a key role for the UPR in normal neuronal function and as an important driver of neurodegenerative diseases. A complex scenario is emerging in which distinct UPR signalling modules have specific and even opposite effects on neurodegeneration depending on the disease context. Here, we provide an overview of the most recent findings addressing the biological relevance of ER stress in the nervous system.

Indexed as

AnimalsEndoplasmic ReticulumHomeostasisHumansNeurodegenerative DiseasesStress, PhysiologicalUnfolded Protein Response

Identifiers

PMID24619348

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.