Evidence map›Paper›PMID 32781522›Full record

ReviewInternational journal of molecular sciences2020

Involvement of p38 MAPK in Synaptic Function and Dysfunction.

Chiara Falcicchia, Francesca Tozzi, Ottavio Arancio, Daniel Martin Watterson, Nicola Origlia

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed, 2 pooled it
12.3field-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

137 citing papers in PubMed, 2 syntheses or guidelines pooled it, 218 citations in OpenAlex.

  1. Pooled it
  2. Proprietary Medicines ContainingFrontiers in pharmacology · 2022
    Pooled it
  3. Review
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  13. Protective Effects of Pomiferin on Aluminum Chloride-induced Memory Impairment: Evidence from Behavioral, Biochemical, and Insilico Studies.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Article
  14. Review
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  16. DIRAS2 modulates MAPK pathway-mediated ferroptosis to regulate excitation/inhibition balance and seizure susceptibility.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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77 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 4 institutions in 2 countries.

Chiara FalcicchiaInstitute of Neuroscience, Italian National Research Council, 56124 Pisa, Italy.ORCID 0000-0002-9648-5713
Francesca TozziBio@SNS laboratory, Scuola Normale Superiore, 56124 Pisa, Italy.
Ottavio ArancioTaub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, NY 10032, USA.
Daniel Martin WattersonDepartment of Pharmacology, Northwestern University, Chicago, IL 60611, USA.
Nicola OrigliaInstitute of Neuroscience, Italian National Research Council, 56124 Pisa, Italy.
National Research Council · ITColumbia University · USNorthwestern University · USScuola Normale Superiore · IT

Funding

Preclinical Alzheimers Disease Drug Development of Novel MAPK InhibitorsU01AG043415 · NIA · NORTHWESTERN UNIVERSITY AT CHICAGO · PI WATTERSON, DANIEL MARTIN · 2012 to 2016
$6.2M
Production and quality analysis of clinical drug for a novel CNS protein kinase inhibitor therapeutic candidateR42AG062095 · NIA · NEUROKINE THERAPEUTICS, LLC · PI WATTERSON, DANIEL MARTIN · 2018 to 2020
$3.2M
NIA NIH HHS R42 AG062095NIA NIH HHS U01 AG043415
6 · The paper itself

Abstract

Many studies have revealed a central role of p38 MAPK in neuronal plasticity and the regulation of long-term changes in synaptic efficacy, such as long-term potentiation (LTP) and long-term depression (LTD). However, p38 MAPK is classically known as a responsive element to stress stimuli, including neuroinflammation. Specific to the pathophysiology of Alzheimer's disease (AD), several studies have shown that the p38 MAPK cascade is activated either in response to the Aβ peptide or in the presence of tauopathies. Here, we describe the role of p38 MAPK in the regulation of synaptic plasticity and its implication in an animal model of neurodegeneration. In particular, recent evidence suggests the p38 MAPK α isoform as a potential neurotherapeutic target, and specific inhibitors have been developed and have proven to be effective in ameliorating synaptic and memory deficits in AD mouse models.

Indexed as

AnimalsBrainHumansInflammationp38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsSmall Molecule LibrariesSynapsesp38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsSmall Molecule LibrariesAlzheimer’s diseaseneuroinflammationp38-MAPK α inhibitorsynaptic plasticityTauβ-amyloid

Identifiers

PMID32781522
PMCPMC7460549
OpenAlexW3047617638

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.