Evidence map›Paper›PMID 34933094›Full record

ArticleNeurobiology of disease2022

Differential effects of mTOR inhibition and dietary ketosis in a mouse model of subacute necrotizing encephalomyelopathy.

Rebecca Bornstein, Katerina James, Julia Stokes, Kyung Yeon Park, Ernst-Bernhard Kayser, John Snell, Angela Bard, Yihan Chen, Franck Kalume, Simon C Johnson

Abstract read
In one paragraph

Article in Neurobiology of disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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

10 citing papers in PubMed.

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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

10 authors.

Rebecca BornsteinDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, United States of America.
Katerina JamesCenter for Integrative Brain Research, Seattle Children's Research Institute, Seattle, WA, United States of America.
Julia StokesCenter for Integrative Brain Research, Seattle Children's Research Institute, Seattle, WA, United States of America.
Kyung Yeon ParkCenter for Integrative Brain Research, Seattle Children's Research Institute, Seattle, WA, United States of America.
Ernst-Bernhard KayserCenter for Integrative Brain Research, Seattle Children's Research Institute, Seattle, WA, United States of America.
John SnellCenter for Integrative Brain Research, Seattle Children's Research Institute, Seattle, WA, United States of America.
Angela BardCenter for Integrative Brain Research, Seattle Children's Research Institute, Seattle, WA, United States of America.
Yihan ChenCenter for Integrative Brain Research, Seattle Children's Research Institute, Seattle, WA, United States of America.
Franck KalumeCenter for Integrative Brain Research, Seattle Children's Research Institute, Seattle, WA, United States of America; Department of Neurological Surgery, University of Washington, Seattle, WA, United States of America. Electronic address: fkalume@uw.edu.
Simon C JohnsonDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, United States of America; Center for Integrative Brain Research, Seattle Children's Research Institute, Seattle, WA, United States of America; Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, WA, United States of America; Department of Neurology, University of Washington, Seattle, WA, United States of America. Electronic address: simoncj@uw.edu.

Funding

Mechanisms of epilepsy-related death in Leigh syndromeR01NS102796 · NINDS · SEATTLE CHILDREN'S HOSPITAL · PI KALUME, FRANCK K · 2017 to 2021
$2.1M
Therapeutic effects of ketogenic diet in mouse model of severe myoclonic epilepsyK01NS062862 · NINDS · UNIVERSITY OF WASHINGTON · PI KALUME, FRANCK K · 2009 to 2013
$804k
The role of mTOR in mitochondrial encephalopathyR00GM126147 · NIGMS · SEATTLE CHILDREN'S HOSPITAL · PI JOHNSON, SIMON C · 2019 to 2021
$747k
Developing approaches for modeling genomic and proteomic profiles in lung cancerR00CA126147 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI MCMAHON, PAMELA MARKELL · 2009 to 2011
$718k
Cerebellar metabolism in mitochondrial diseaseF31NS120442 · NINDS · SEATTLE CHILDREN'S HOSPITAL · PI BORNSTEIN, REBECCA · 2021 to 2021
$43k
NCI NIH HHS R00 CA126147NIGMS NIH HHS R00 GM126147NINDS NIH HHS F31 NS120442NINDS NIH HHS K01 NS062862NINDS NIH HHS R01 NS102796
6 · The paper itself

Abstract

Genetic mitochondrial diseases are the most frequent cause of inherited metabolic disorders and one of the most prevalent causes of heritable neurological disease. Leigh syndrome is the most common clinical presentation of pediatric mitochondrial disease, typically appearing in the first few years of life, and involving severe multisystem pathologies. Clinical care for Leigh syndrome patients is difficult, complicated by the wide range of symptoms including characteristic progressive CNS lesion, metabolic sequelae, and epileptic seizures, which can be intractable to standard management. While no proven therapies yet exist for the underlying mitochondrial disease, a ketogenic diet has led to some reports of success in managing mitochondrial epilepsies, with ketosis reducing seizure risk and severity. The impact of ketosis on other aspects of disease progression in Leigh syndrome has not been studied, however, and a rigorous study of the impact of ketosis on seizures in mitochondrial disease is lacking. Conversely, preclinical efforts have identified the intracellular nutrient signaling regulator mTOR as a promising therapeutic target, with data suggesting the benefits are mediated by metabolic changes. mTOR inhibition alleviates epilepsies arising from defects in TSC, an mTOR regulator, but the therapeutic potential of mTOR inhibition in seizures related to primary mitochondrial dysfunction is unknown. Given that ketogenic diet is used clinically in the setting of mitochondrial disease, and mTOR inhibition is in clinical trials for intractable pediatric epilepsies of diverse causal origins, a direct experimental assessment of their effects is imperative. Here, we define the impact of dietary ketosis on survival and CNS disease in the Ndufs4(KO) mouse model of Leigh syndrome and the therapeutic potential of both dietary ketosis and mTOR inhibition on seizures in this model. These data provide timely insight into two important clinical interventions.

Indexed as

Diet, KetogenicAnimalsDisease Models, AnimalElectron Transport Complex ILeigh DiseaseMiceMice, KnockoutSirolimusTOR Serine-Threonine KinasesTreatment OutcomeElectron Transport Complex IMTOR protein, humanNdufs4 protein, mouseSirolimusTOR Serine-Threonine KinasesEpilepsyKetogenic dietKetosisMitochondrial diseasemTORSeizure

Identifiers

PMID34933094
PMCPMC8770160

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.