Evidence mapPaperPMID 31913484Full record

ReviewJournal of neuropathology and experimental neurology2020

The Integrated Stress Response and Phosphorylated Eukaryotic Initiation Factor 2α in Neurodegeneration.

Sarah Bond, Claudia Lopez-Lloreda, Patrick J Gannon, Cagla Akay-Espinoza, Kelly L Jordan-Sciutto

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of neuropathology and experimental neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
9.9field-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

81 citing papers in PubMed, 134 citations in OpenAlex.

  1. Distinct cell type-specific mechanisms underlie cognitive dysfunction during persistent integrated stress response activation.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  19. Inflammatory cytokine upd3 induces axon length-dependent synapse removal by glia.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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21 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

5 authors at 1 institution in 1 country.

Sarah BondFrom the Department of Biochemistry and Biophysics (SB); Department of Neuroscience (CL-L); Department of Pharmacology (PG), Perelman School of Medicine; Department of Basic and Translational Sciences (CA-E); and Department of Basic and Translational Sciences (KLJ-S), School of Dental Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Claudia Lopez-LloredaFrom the Department of Biochemistry and Biophysics (SB); Department of Neuroscience (CL-L); Department of Pharmacology (PG), Perelman School of Medicine; Department of Basic and Translational Sciences (CA-E); and Department of Basic and Translational Sciences (KLJ-S), School of Dental Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Patrick J GannonFrom the Department of Biochemistry and Biophysics (SB); Department of Neuroscience (CL-L); Department of Pharmacology (PG), Perelman School of Medicine; Department of Basic and Translational Sciences (CA-E); and Department of Basic and Translational Sciences (KLJ-S), School of Dental Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Cagla Akay-EspinozaFrom the Department of Biochemistry and Biophysics (SB); Department of Neuroscience (CL-L); Department of Pharmacology (PG), Perelman School of Medicine; Department of Basic and Translational Sciences (CA-E); and Department of Basic and Translational Sciences (KLJ-S), School of Dental Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Kelly L Jordan-SciuttoFrom the Department of Biochemistry and Biophysics (SB); Department of Neuroscience (CL-L); Department of Pharmacology (PG), Perelman School of Medicine; Department of Basic and Translational Sciences (CA-E); and Department of Basic and Translational Sciences (KLJ-S), School of Dental Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
University of Pennsylvania · US

Funding

PREDOCTORAL TRAINING PROGRAM IN PHARMACOLOGYT32GM008076 · UNIVERSITY OF PENNSYLVANIA · 1985 to 2005
$2.0M
STRUCTURAL BIOLOGY TRAINING PROGRAMT32GM008275 · UNIVERSITY OF PENNSYLVANIA · 1988 to 2005
$1.7M
Translational Research Support CoreP30ES013508 · UNIVERSITY OF PENNSYLVANIA · 2025 to 2025
$1.6M
Oligodendrocyte damage and dysfunction in HIV associated neurocognitive disorderR01MH098742 · NIMH · UNIVERSITY OF PENNSYLVANIA · 2022 to 2025
$1.4M
NIDA NIH HHS R01 DA049514NIEHS NIH HHS P30 ES013508NIGMS NIH HHS T32 GM008076NIGMS NIH HHS T32 GM008275NIMH NIH HHS R01 MH083517NIMH NIH HHS R01 MH098742NIMH NIH HHS R01 MH106967NIMH NIH HHS R01 MH109382NINDS NIH HHS R01 NS056885
6 · The paper itself

Abstract

The proposed molecular mechanisms underlying neurodegenerative pathogenesis are varied, precluding the development of effective therapies for these increasingly prevalent disorders. One of the most consistent observations across neurodegenerative diseases is the phosphorylation of eukaryotic initiation factor 2α (eIF2α). eIF2α is a translation initiation factor, involved in cap-dependent protein translation, which when phosphorylated causes global translation attenuation. eIF2α phosphorylation is mediated by 4 kinases, which, together with their downstream signaling cascades, constitute the integrated stress response (ISR). While the ISR is activated by stresses commonly observed in neurodegeneration, such as oxidative stress, endoplasmic reticulum stress, and inflammation, it is a canonically adaptive signaling cascade. However, chronic activation of the ISR can contribute to neurodegenerative phenotypes such as neuronal death, memory impairments, and protein aggregation via apoptotic induction and other maladaptive outcomes downstream of phospho-eIF2α-mediated translation inhibition, including neuroinflammation and altered amyloidogenic processing, plausibly in a feed-forward manner. This review examines evidence that dysregulated eIF2a phosphorylation acts as a driver of neurodegeneration, including a survey of observations of ISR signaling in human disease, inspection of the overlap between ISR signaling and neurodegenerative phenomenon, and assessment of recent encouraging findings ameliorating neurodegeneration using developing pharmacological agents which target the ISR. In doing so, gaps in the field, including crosstalk of the ISR kinases and consideration of ISR signaling in nonneuronal central nervous system cell types, are highlighted.

Indexed as

Stress, PhysiologicalAnimalsEukaryotic Initiation Factor-2Gene Expression RegulationHumansNeurodegenerative DiseasesPhosphorylationSignal TransductionEIF2S1 protein, humanEukaryotic Initiation Factor-2Cell fateeIF2αIntegrated stress response (ISR)NeurodegenerationNeurodegenerative disease pathogenesisphosphorylation (p-eIF2α)Stress signaling

Identifiers

PMID31913484
PMCPMC6970450
OpenAlexW2999291506

What Socratic 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 Socratic graph.