ReviewProgress in molecular biology and translational science2020
The putative etiology and prevention of autism.
Review in Progress in molecular biology and translational science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled 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.
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
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Pooled it
- Risk factors for autism spectrum disorder among infants and children admitted in a neonatal intensive care unit.Dialogues in health · 2026Article
- Placental Insulin-like Growth Factor 1 Insufficiency Drives Neurodevelopmental Disorder-Relevant Behavioral Changes with Sex-Specific Vulnerabilities.bioRxiv : the preprint server for biology · 2026Article
- Placental Igf1 overexpression sex-specifically impacts mouse placenta structure, altering offspring striatal development and behavior.Experimental neurology · 2025Article
- A head start: The relationship of placental factors to craniofacial and brain development.Developmental dynamics : an official publication of the American Association of Anatomists · 2025Review
- A dataset of adult heart and liver mass after placentalbioRxiv : the preprint server for biology · 2025Article
- Molecular architecture of the altered cortical complexity in autism.Molecular autism · 2025Article
- Oxytocin enhances oligodendrocyte development and improves social deficits in autistic rats.Frontiers in neuroscience · 2025Article
- The association between IGF-1 levels and four types of osteoarthritis: a bidirectional and two-step mendelian randomization study.Frontiers in genetics · 2024Article
- How (and why) languages became more complex as we evolved more prosocial: the human self-domestication view.Frontiers in psychology · 2024Article
- Potential Benefits of Anthocyanins in Chronic Disorders of the Central Nervous System.Molecules (Basel, Switzerland) · 2022Review
- Immune Dysregulation in Autism Spectrum Disorder: What Do We Know about It?International journal of molecular sciences · 2022Review
- Dynamic and Systemic Perspective in Autism Spectrum Disorders: A Change of Gaze in Research Opens to A New Landscape of Needs and Solutions.Brain sciences · 2022Review
- Research Progress on the Role of Vitamin D in Autism Spectrum Disorder.Frontiers in behavioral neuroscience · 2022Review
- Prevention in Autism Spectrum Disorder: A Lifelong Focused Approach.Brain sciences · 2021Review
- Systemic Inflammation and Astrocyte Reactivity in the Neuropsychiatric Sequelae of COVID-19: Focus on Autism Spectrum Disorders.Frontiers in cellular neuroscience · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Since the initial psychological report by Leo Kanner in 1943, relatively little formal biochemical/neurological research on the cause of autism, other than peripheral searches for genomic mutations, had been carried until the end of the 20th century. As a result of studies on twin sets and the conclusion that autism was largely a hereditary defect, numerous investigations have sought various genetic faults in particular. However, such studies were able to reveal a plausible etiology for this malady in only a small percentage of instances. Key bio-molecular characteristics of this syndrome have been uncovered when the potential roles of the glia were studied in depth. Findings related to biochemical deficiencies appearing early in the newborn, such as depressed IGF-1 (insulin-like growth factor #1) in neurogenesis/myelination, are becoming emphasized in many laboratories. Progress leading to timely diagnoses and subsequent prevention of central nervous system dysconnectivity now seems plausible. The tendency for an infant to develop autism may currently be determinable and preventable before irreversible psychosocial disturbances become established. These discussions about glial function will be inter-spersed with comments about their apparent relevance to autism. The concluding portion of this presentation will be a detailed review and summation of this diagnosis and prevention proposition.
Indexed as
Identifiers
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.