ReviewMolecular autism2018
Autism spectrum disorder: prospects for treatment using gene therapy.
Review in Molecular autism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 65 citations in OpenAlex.
- Linking rare variants to cell-type function in profound autism with brain transcriptomics and foundation models.Cell genomics · 2026Review
- Remimazolam Ameliorates Autistic-Like Behaviors via Suppression of Ferroptosis in VTA Dopaminergic Neurons in a Mouse Model of ASD.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The emerging role of gene therapy in autism spectrum disorder.Discover mental health · 2026Review
- Does Altered Membrane Glycosylation Contribute to Neurodevelopmental Dysfunction in Autism Spectrum Disorder?Membranes · 2026Review
- Membrane Trafficking in Psychiatric Disorders: Bridging Cellular Dysfunction and Mental Health-A Narrative Review.Molecular neurobiology · 2025Review
- Article
- Autism spectrum disorder and the role of nuclear hormone receptors: insights and therapeutic implications.Frontiers in neuroscience · 2025Review
- EF1α-associated protein complexes affect dendritic spine plasticity by regulating microglial phagocytosis in Fmr1 knock-out mice.Molecular psychiatry · 2024Article
- Suppression of Cofilin function in the somatosensory cortex alters social contact behavior in the BTBR mouse inbred line.Cerebral cortex (New York, N.Y. : 1991) · 2024Article
- Synthetic dosage-compensating miRNA circuits allow precision gene therapy for Rett syndrome.bioRxiv : the preprint server for biology · 2024Article
- Diversity and Classification of Genetic Variations in Autism Spectrum Disorder.International journal of molecular sciences · 2023Review
- Therapeutic strategies for autism: targeting three levels of the central dogma of molecular biology.Translational psychiatry · 2023Review
- How to Make the Unpredictable Foreseeable? Effective Forms of Assistance for Children with Autism Spectrum Disorder (ASD) during the COVID-19 Pandemic.Diagnostics (Basel, Switzerland) · 2023Review
- Canagliflozin alleviates valproic acid-induced autism in rat pups: Role of PTEN/PDK/PPAR-γ signaling pathways.Frontiers in pharmacology · 2023Article
- Small Nucleus Accumbens and Large Cerebral Ventricles in Infants and Toddlers Prior to Receiving Diagnoses of Autism Spectrum Disorder.Cerebral cortex (New York, N.Y. : 1991) · 2022Article
- Molecular mechanisms of synaptogenesis.Frontiers in synaptic neuroscience · 2022Review
- Review
- Genetic contributions to autism spectrum disorder.Psychological medicine · 2021Review
- An Update on Precision Medicine Advances In Neurodevelopmental Disorders.Psychiatric annals · 2021Article
- Improvement of autistic-like behaviors in adult rats prenatally exposed to valproic acid through early suppression of NMDA receptor function.Psychopharmacology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autism spectrum disorder (ASD) is characterised by the concomitant occurrence of impaired social interaction; restricted, perseverative and stereotypical behaviour; and abnormal communication skills. Recent epidemiological studies have reported a dramatic increase in the prevalence of ASD with as many as 1 in every 59 children being diagnosed with ASD. The fact that ASD appears to be principally genetically driven, and may be reversible postnatally, has raised the exciting possibility of using gene therapy as a disease-modifying treatment. Such therapies have already started to seriously impact on human disease and particularly monogenic disorders (e.g. metachromatic leukodystrophy, SMA type 1). In regard to ASD, technical advances in both our capacity to model the disorder in animals and also our ability to deliver genes to the central nervous system (CNS) have led to the first preclinical studies in monogenic ASD, involving both gene replacement and silencing. Furthermore, our increasing awareness and understanding of common dysregulated pathways in ASD have broadened gene therapy's potential scope to include various polygenic ASDs. As this review highlights, despite a number of outstanding challenges, gene therapy has excellent potential to address cognitive dysfunction in ASD.
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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.