Evidence map›Paper›PMID 28270747›Full record

ReviewFrontiers in molecular neuroscience2017

Metabolic Dysfunction Underlying Autism Spectrum Disorder and Potential Treatment Approaches.

Ning Cheng, Jong M Rho, Susan A Masino

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 3 pooled it
6.4field-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

75 citing papers in PubMed, 3 syntheses or guidelines pooled it, 141 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review

15 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

3 authors at 2 institutions in 2 countries.

Ning ChengDepartments of Pediatrics, University of Calgary Calgary, AB, Canada.
Jong M RhoDepartments of Pediatrics, University of CalgaryCalgary, AB, Canada; Clinical Neurosciences, University of CalgaryCalgary, AB, Canada; Physiology and Pharmacology, Alberta Children's Hospital Research Institute, Cumming School of Medicine, University of CalgaryCalgary, AB, Canada.
Susan A MasinoNeuroscience Program, Department of Psychology, Trinity College Hartford, CT, USA.
University of Calgary · CATrinity College · US

Funding

The Role of Adenosine in Ketogenic Diet TherapyR01NS065957 · NINDS · TRINITY COLLEGE · PI BOISON, DETLEV, GEIGER, JONATHAN DAVID · 2010 to 2021
$3.9M
Ketogentic diet-induced changes in the cerebrospinal fluid: biomarkers and mechanismsR15NS066392 · NINDS · TRINITY COLLEGE · PI MASINO, SUSAN A · 2010 to 2015
$583k
NINDS NIH HHS R01 NS065957NINDS NIH HHS R15 NS066392
6 · The paper itself

Abstract

Autism spectrum disorder (ASD) is characterized by deficits in sociability and communication, and increased repetitive and/or restrictive behaviors. While the etio-pathogenesis of ASD is unknown, clinical manifestations are diverse and many possible genetic and environmental factors have been implicated. As such, it has been a great challenge to identify key neurobiological mechanisms and to develop effective treatments. Current therapies focus on co-morbid conditions (such as epileptic seizures and sleep disturbances) and there is no cure for the core symptoms. Recent studies have increasingly implicated mitochondrial dysfunction in ASD. The fact that mitochondria are an integral part of diverse cellular functions and are susceptible to many insults could explain how a wide range of factors can contribute to a consistent behavioral phenotype in ASD. Meanwhile, the high-fat, low-carbohydrate ketogenic diet (KD), used for nearly a century to treat medically intractable epilepsy, has been shown to enhance mitochondrial function through a multiplicity of mechanisms and affect additional molecular targets that may address symptoms and comorbidities of ASD. Here, we review the evidence for the use of metabolism-based therapies such as the KD in the treatment of ASD as well as emerging co-morbid models of epilepsy and autism. Future research directions aimed at validating such therapeutic approaches and identifying additional and novel mechanistic targets are also discussed.

Indexed as

autism spectrum disorderco-morbidityepilepsyketogenic dietmechanismmetabolismmitochondriatherapeutics

Identifiers

PMID28270747
PMCPMC5318388
OpenAlexW2591444651

What Socratic 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 Socratic graph.