Evidence map›Paper›PMID 32036255›Full record

ReviewEpilepsy research2020

Therapeutic role of targeting mTOR signaling and neuroinflammation in epilepsy.

Samantha L Hodges, Joaquin N Lugo

Open access · greenAbstract readReview
In one paragraph

Review in Epilepsy research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 2 pooled it
5.1field-weighted citation impact, top 3% 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

61 citing papers in PubMed, 2 syntheses or guidelines pooled it, 81 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  12. Article
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  18. Translocator protein (18 kDa) positron emission tomography imaging as a biomarker of neuroinflammation in epilepsy.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
    Review
  19. Article
  20. Anti‑epileptic mechanism of isopimaric acid fromExperimental and therapeutic medicine · 2024
    Article

1 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 at 1 institution in 1 country.

Samantha L HodgesInstitute of Biomedical Studies, Baylor University, Waco, TX 76798, USA.
Joaquin N LugoInstitute of Biomedical Studies, Baylor University, Waco, TX 76798, USA; Department of Psychology and Neuroscience, Baylor University, Waco, TX 76798, USA; Department of Biology, Baylor University, Waco, TX 76798, USA. Electronic address: joaquin_lugo@baylor.edu.
Baylor University · US

Funding

Signaling Mechanisms Underlying Epilepsy and Autism CormorbidityR15NS088776 · NINDS · BAYLOR UNIVERSITY · PI JOAQUIN N LUGO · 2015 to 2026
$1.8M
NINDS NIH HHS R15 NS088776
6 · The paper itself

Abstract

Existing therapies for epilepsy are primarily symptomatic and target mechanisms of neuronal transmission in order to restore the excitatory/inhibitory imbalance in the brain after seizures. However, approximately one third of individuals with epilepsy have medically refractory epilepsy and do not respond to available treatments. There is a critical need for the development of therapeutics that extend beyond manipulation of excitatory neurotransmission and target pathological changes underlying the cause of the disease. Epilepsy is a multifaceted condition, and it could be that effective treatment involves the targeting of several mechanisms. There is evidence for both dysregulated PI3K/Akt/mTOR (mTOR) signaling and heightened neuroinflammatory processes following seizures in the brain. Signaling via mTOR has been implicated in several epileptogenic processes, including synaptic plasticity mechanisms and changes in ion channel expression following seizures. Inflammatory signaling, such as increased synthesis of cytokines and other immune molecules, has also shown to play a significant role in the development of chronic epilepsy. mTOR pathway activation and immune signaling are known to interact in normal physiological states, as well as influence one another following seizures. Simultaneous inhibition of both processes could be a promising therapeutic avenue to prevent the development of chronic epilepsy by targeting two key pathological mechanisms implicated in epileptogenesis.

Indexed as

AnimalsBrainEpilepsyHumansPhosphatidylinositol 3-KinasesSeizuresSignal TransductionTOR Serine-Threonine KinasesPhosphatidylinositol 3-KinasesTOR Serine-Threonine KinasesCytokinesEpileptogenesisInflammationmTORRapamycinSeizures

Identifiers

PMID32036255
PMCPMC9205332
OpenAlexW3003340868

What Socratic 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 Socratic graph.