Evidence map›Paper›PMID 32165256›Full record

ReviewExperimental neurology2020

Crosstalk between the mTOR and Nrf2/ARE signaling pathways as a target in the improvement of long-term potentiation.

Artem P Gureev, Vasily N Popov, Anatoly A Starkov

Open access · greenAbstract readReview
In one paragraph

Review in Experimental neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

33 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Overexpression ofInternational journal of molecular sciences · 2026
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  12. Allicin: a promising modulator of apoptosis and survival signaling in cancer.Medical oncology (Northwood, London, England) · 2024
    Review
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  20. The Interaction ofCells · 2022
    Review
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

3 authors at 3 institutions in 2 countries.

Artem P GureevDepartment of Genetics, Cytology and Bioengineering, Voronezh State University, Voronezh, Russia.
Vasily N PopovDepartment of Genetics, Cytology and Bioengineering, Voronezh State University, Voronezh, Russia; Voronezh State University of Engineering Technologies, Voronezh, Russia.
Anatoly A StarkovFeil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY, USA. Electronic address: ans2024@med.cornell.edu.
Cornell University · USVoronezh State University · RUVoronezh State University of Engineering Technologies · RU

Funding

TRANSCRIPTIONAL RESPONSES TO MITOCHONDRIAL DYSFUNCTIONP01AG014930 · NIA · WINIFRED MASTERSON BURKE MED RES INST · PI GIBSON, GARY E · 1999 to 2020
$30.7M
NIA NIH HHS P01 AG014930
6 · The paper itself

Abstract

In recent years, a significant progress was made in understanding molecular mechanisms of long-term memory. Long-term memory formation requires strengthening of neuronal connections (LTP, long-term potentiation) associated with structural rearrangement of neurons. The key role in the synthesis of proteins essential for these rearrangements belong to mTOR (mammalian target of rapamycin) complexes and signaling pathways involved in mTOR regulation. Suppression of mTOR activity may impair synaptic plasticity and long-term memory, while mTOR activation inhibits autophagy, thereby potentiating amyloidosis and development of Alzheimer's disease (AD) accompanied by irreversible memory loss. Because of this, suppression/inhibition of mTOR might have unpredictable consequences on memory. The Nrf2/ARE signaling pathway affects almost all mitochondrial processes. The activation of this pathway improves memory and exhibits therapeutic effect in AD. In this review, we discuss the crosstalk between the Nrf2/ARE signaling and mTOR in the maintenance of synaptic plasticity. Nrf2 pathway can be activated by pharmacological agents and by changes in mitochondria functioning accompanying various neuronal dysfunctions.

Indexed as

AnimalsAntioxidant Response ElementsHumansLong-Term PotentiationMemory, Long-TermNF-E2-Related Factor 2Receptor Cross-TalkSignal TransductionTOR Serine-Threonine KinasesNF-E2-Related Factor 2TOR Serine-Threonine KinasesAlzheimer's diseaseLong term memorymTORNeuronsNrf2

Identifiers

PMID32165256
PMCPMC7145749
OpenAlexW3011794336

What OpenQuestion holds

Textmetadata
LicenceTDM
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.