Evidence map›Paper›PMID 31838997›Full record

ReviewJournal of neurodevelopmental disorders2019

The role of glia in epilepsy, intellectual disability, and other neurodevelopmental disorders in tuberous sclerosis complex.

Michael Wong

Open access · goldAbstract readReview
In one paragraph

Review in Journal of neurodevelopmental disorders, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

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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

1 author at 1 institution in 1 country.

Michael WongDepartment of Neurology and the Hope Center for Neurological Disorders, Washington University School of Medicine, 660 South Euclid Avenue, Box 8111, St. Louis, MO, 63110, USA. wong_m@wustl.edu.ORCID 0000-0002-3796-743X
Hope Center for Neurological Disorders · US

Funding

Washington University Intellectual and Developmental Disabilities Research Center-Administrative Down Syndrome SupplementU54HD087011 · NICHD · WASHINGTON UNIVERSITY · PI CONSTANTINO, JOHN N. · 2015 to 2019
$7.1M
MECHANISMS OF BRAIN DYSFUNCTION IN TUBEROUS SCLEROSISR01NS056872 · NINDS · WASHINGTON UNIVERSITY · PI WONG, MICHAEL · 2006 to 2019
$4.0M
NICHD NIH HHS U54 HD087011NINDS NIH HHS R01 NS056872NINDS NIH HHS U54 HD087011
6 · The paper itself

Abstract

backgroundTuberous sclerosis complex (TSC) is a genetic disorder characterized by severe neurological manifestations, including epilepsy, intellectual disability, autism, and a range of other behavioral and psychiatric symptoms, collectively referred to as TSC-associated neuropsychiatric disorders (TAND). Various tumors and hamartomas affecting different organs are the pathological hallmarks of the disease, especially cortical tubers of the brain, but specific cellular and molecular abnormalities, such as involving the mechanistic target of rapamycin (mTOR) pathway, have been identified that also cause or contribute to neurological manifestations of TSC independent of gross structural lesions. In particular, while neurons are immediate mediators of neurological symptoms, different types of glial cells have been increasingly recognized to play important roles in the phenotypes of TSC. MAIN BODY: This review summarizes the literature supporting glial dysfunction from both mouse models and clinical studies of TSC. In particular, evidence for the role of astrocytes, microglia, and oligodendrocytes in the pathophysiology of epilepsy and TAND in TSC is analyzed. Therapeutic implications of targeting glia cells in developing novel treatments for the neurological manifestations of TSC are also considered.

conclusionsDifferent types of glial cells have both cell autonomous effects and interactions with neurons and other cells that are involved in the pathophysiology of the neurological phenotype of TSC. Targeting glial-mediated mechanisms may represent a novel therapeutic approach for epilepsy and TAND in TSC patients.

Indexed as

AnimalsBrainEpilepsyHumansIntellectual DisabilityNeurodevelopmental DisordersNeurogliaNeuronsTuberous SclerosisAstrocyteAutism spectrum disorderEpilepsyGliaIntellectual disabilityMicrogliaOligodendrocyteTANDTuberous sclerosisWhite matter

Identifiers

PMID31838997
PMCPMC6913020
OpenAlexW2996094946

What OpenQuestion holds

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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.