Pubmed (TSA) du 19/01/26
1. Keating CT, Sowden-Carvalho S, H OD, Cook JL. Mismatching Expressions: Spatiotemporal and Kinematic Differences in Autistic and Non-Autistic Facial Expressions. Autism Res;2026 (Jan 18)
Preliminary studies suggest there are differences in the facial expressions produced by autistic and non-autistic individuals. However, it is unclear what specifically is different, whether such differences remain after controlling for facial morphology and alexithymia, and whether production differences relate to perception differences. Therefore, we (1) comprehensively compared the spatiotemporal and kinematic properties of autistic and non-autistic expressions after controlling these factors, and (2) examined the contribution of production-related variables to emotion perception. We used facial motion capture to record 2448 cued and 2448 spoken expressions of anger, happiness, and sadness from autistic and matched non-autistic adults. Subsequently, we extracted the activation and jerkiness of numerous facial landmarks across time, generating over 265 million datapoints. Participants also completed an emotion recognition task. Autistic participants relied more on the mouth, and less on the eyebrows, to signal anger than their non-autistic peers. For happiness, autistic participants showed a less exaggerated smile that also did not « reach the eyes. » For sadness, autistic participants tended to produce a downturned expression by raising their upper lip more than their non-autistic peers. Alexithymia predicted less differentiated angry and happy expressions. For non-autistic individuals, those who produced more precise spoken expressions had greater emotion recognition accuracy. No production-related factors contributed to autistic emotion recognition. This mismatch could explain why autistic people find it difficult to recognize non-autistic expressions, and vice versa; autistic and non-autistic faces may be essentially « speaking a different language » when conveying emotion. This study compared the facial expressions produced by autistic and non‐autistic people. Our findings demonstrate that autistic and non‐autistic adults produce different angry, happy, and sad facial expressions, even after accounting for other interfering factors. This mismatch in facial expressions could explain why autistic people find it difficult to recognize non‐autistic expressions, and vice versa; autistic and non‐autistic faces may be essentially “speaking a different language” when it comes to conveying emotion. As such, what have previously been thought of as intrinsic emotion recognition “deficits” for autistic people may be more accurately described as difficulties resulting from cross‐neurotype interactions (i.e., interactions between autistic and non‐autistic people, as opposed to interactions between two autistic people). Further research is needed to test the impact of expressive differences on emotion recognition for autistic and non‐autistic people. eng
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2. Munir KM. Etiology of autism spectrum disorders: recent advances and emerging directions. Curr Opin Psychiatry;2026 (Jan 19)
PURPOSE OF REVIEW: This narrative review synthesizes advances from the past 18 months on the etiology of autism spectrum disorder (ASD), integrating findings from genetics, neurobiology, environmental epidemiology, and developmental psychiatry. Given the profound clinical heterogeneity of ASD, improved etiologic clarity is essential for risk stratification, early identification, and targeted intervention. RECENT FINDINGS: Extensive genomic and multiancestry studies are now further clarifying how both common polygenic and rare high-impact variants contribute to ASD. These studies reveal different patterns of genetic liability that underlie distinct ASD subgroups. In parallel, functional and multiomic research is highlighting shared pathways involving synaptic signaling, gene regulation, immune processes, and the balance between excitatory and inhibitory signals. Environmental research, especially on maternal immune activation and maternal metabolic factors, uses causal inference methods to clarify modest but plausible causal effects, tempering earlier claims. Longitudinal imaging and infant cohort studies continue to show that atypical connectivity and social-brain differences occur before behavioral diagnosis. Sex differences and global diversity underscore the need for etiology models to incorporate sex-specific genetic architecture and address significant gaps in ancestral representation. SUMMARY: ASD arises from a dynamic interplay of genetic liability, early neurodevelopmental processes, and environmental exposures. Etiologic progress now depends on integrating multilevel and multiomic data – including genomic, transcriptomic, epigenetic, imaging, and epidemiologic information – toward stratified developmental models and better-tailored interventions.
