ArticleFrontiers in psychiatry2021
A Unifying Theory for Autism: The Pathogenetic Triad as a Theoretical Framework.
Article in Frontiers in psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 18 citations in OpenAlex.
- Broader autism phenotype, the default mode network, and brain entropy: A network-level hypothesis.Research in neurodiversity · 2026Article
- Neural Sensitivity to Conversational Inter-Speaker Gaps in the Broad Autism Phenotype.Psychophysiology · 2026Article
- Integrating Ultimate and Proximate Explanations of Neurodivergence: Evolutionary Trade-Offs, Compensation, and Clinical Expression.Evolutionary applications · 2026Article
- Common molecular signatures: the role of BDNF, melatonin, and orexin in the ASD-schizophrenia continuum.Molecular biology reports · 2026Review
- Generalized environmental fear hypothesis and the effects of schematic restructuring in autism.Frontiers in psychiatry · 2026Article
- Preliminary testing of a prespecified liability architecture for autism: theory-guided pathogenetic triad models outperform strength-matched alternatives.Frontiers in psychiatry · 2026Article
- Structured clinical diagnostic assessment reveals autism spectrum disorder in adults with functional neurological disorder.Scientific reports · 2025Article
- Unique models of embodied cognition and eco-social niches proposed to validate hypothesis of social attunement and mis-attunement with a focus on autism.Frontiers in psychiatry · 2025Article
- Differential late-stage face processing in autism: a magnetoencephalographic study of fusiform gyrus activation.BMC psychiatry · 2024Article
- Functional Neurological Disorder and Autism Spectrum Disorder: A Complex and Potentially Significant Relationship.Brain and behavior · 2024Review
- Animal Models of Autistic-like Behavior in Rodents: A Scoping Review and Call for a Comprehensive Scoring System.International journal of molecular sciences · 2024Article
- Commentary: Autism: A model of neurodevelopmental diversity informed by genomics.Frontiers in psychiatry · 2023Article
- Neurocognitive and cerebellar function in ADHD, autism and spinocerebellar ataxia.Frontiers in systems neuroscience · 2023Review
- Autism Spectrum as an Etiologic Systemic Disorder: A Protocol for an Umbrella Review.Healthcare (Basel, Switzerland) · 2022Article
- Integrating the Autistic Experience Into Existing Models for Disordered Eating.Frontiers in psychology · 2022Article
- Orexin/Hypocretin System Dysfunction in ESSENCE (Early Symptomatic Syndromes Eliciting Neurodevelopmental Clinical Examinations).Neuropsychiatric disease and treatment · 2022Article
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
This paper presents a unifying theory for autism by applying the framework of a pathogenetic triad to the scientific literature. It proposes a deconstruction of autism into three contributing features (an autistic personality dimension, cognitive compensation, and neuropathological risk factors), and delineates how they interact to cause a maladaptive behavioral phenotype that may require a clinical diagnosis. The autistic personality represents a common core condition, which induces a set of behavioral issues when pronounced. These issues are compensated for by cognitive mechanisms, allowing the individual to remain adaptive and functional. Risk factors, both exogenous and endogenous ones, show pathophysiological convergence through their negative effects on neurodevelopment. This secondarily affects cognitive compensation, which disinhibits a maladaptive behavioral phenotype. The triad is operationalized and methods for quantification are presented. With respect to the breadth of findings in the literature that it can incorporate, it is the most comprehensive model yet for autism. Its main implications are that (1) it presents the broader autism phenotype as a non-pathological core personality domain, which is shared across the population and uncoupled from associated features such as low cognitive ability and immune dysfunction, (2) it proposes that common genetic variants underly the personality domain, and that rare variants act as risk factors through negative effects on neurodevelopment, (3) it outlines a common pathophysiological mechanism, through inhibition of neurodevelopment and cognitive dysfunction, by which a wide range of endogenous and exogenous risk factors lead to autism, and (4) it suggests that contributing risk factors, and findings of immune and autonomic dysfunction are clinically ascertained rather than part of the core autism construct.
Indexed as
Identifiers
What Socratic 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 Socratic graph.