ReviewFrontiers in neuroscience2015
Characterizing autism spectrum disorders by key biochemical pathways.
Review in Frontiers in neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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.
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.
Who cites it
43 citing papers in PubMed, 72 citations in OpenAlex.
- Randomized controlled trial of sulforaphane and metabolite discovery in children with Autism Spectrum Disorder.Molecular autism · 2021Trial
- Targeting the mTOR Pathway with Natural Products: A Potential Therapeutic Approach for Autism Spectrum Disorders.Current neuropharmacology · 2026Review
- Innovative biomarker exploration in ASD: Combining Graph Neural Networks and permutation testing on fMRI data.Neuroimage. Reports · 2025Article
- Review
- The MNK-SYNGAP1 axis in specific learning disorder: gene expression pattern and new perspectives.European journal of pediatrics · 2025Article
- Whole-genome sequencing analysis of Japanese autism spectrum disorder trios.Psychiatry and clinical neurosciences · 2025Article
- Nebulized vasopressin penetrates CSF and improves social cognition without inducing aggression in a rhesus monkey model of autism.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Growth-suppressor microRNAs mediate synaptic overgrowth and behavioral deficits in Fragile X mental retardation protein deficiency.iScience · 2024Article
- Three Decades of Valproate: A Current Model for Studying Autism Spectrum Disorder.Current neuropharmacology · 2024Review
- Tales from the life and lab of a female social neuroscientist.Comprehensive psychoneuroendocrinology · 2023Review
- Recent advances to Neuroprotection: repurposing drugs against neuroinflammatory disorders.Molecular biology reports · 2023Review
- Therapeutic modulation of JAK-STAT, mTOR, and PPAR-γ signaling in neurological dysfunctions.Journal of molecular medicine (Berlin, Germany) · 2023Review
- APPlications of amyloid-β precursor protein metabolites in macrocephaly and autism spectrum disorder.Frontiers in molecular neuroscience · 2023Review
- Autism spectrum disorder in the fragile X premutation state: possible mechanisms and implications.Journal of neurology · 2022Review
- Leveraging a translational research approach to drive diagnostic and treatment advances for autism.Molecular psychiatry · 2022Review
- Article
- Review
- DNA Methylation of the Oxytocin Receptor Across Neurodevelopmental Disorders.Journal of autism and developmental disorders · 2021Article
- Autism Spectrum Disorder: Signaling Pathways and Prospective Therapeutic Targets.Cellular and molecular neurobiology · 2021Review
- Non-Syndromic Intellectual Disability and Its Pathways: A Long Noncoding RNA Perspective.Non-coding RNA · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The genetic and phenotypic heterogeneity of autism spectrum disorders (ASD) presents a substantial challenge for diagnosis, classification, research, and treatment. Investigations into the underlying molecular etiology of ASD have often yielded mixed and at times opposing findings. Defining the molecular and biochemical underpinnings of heterogeneity in ASD is crucial to our understanding of the pathophysiological development of the disorder, and has the potential to assist in diagnosis and the rational design of clinical trials. In this review, we propose that genetically diverse forms of ASD may be usefully parsed into entities resulting from converse patterns of growth regulation at the molecular level, which lead to the correlates of general synaptic and neural overgrowth or undergrowth. Abnormal brain growth during development is a characteristic feature that has been observed both in children with autism and in mouse models of autism. We review evidence from syndromic and non-syndromic ASD to suggest that entities currently classified as autism may fundamentally differ by underlying pro- or anti-growth abnormalities in key biochemical pathways, giving rise to either excessive or reduced synaptic connectivity in affected brain regions. We posit that this classification strategy has the potential not only to aid research efforts, but also to ultimately facilitate early diagnosis and direct appropriate therapeutic interventions.
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What OpenQuestion holds
Registered trials
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.