1. García-Fernández D, de Santos B, López-Diego D, Luna M, González-Tobío B, Mateo-Martí E, Zamora F, Cabrera S, Aleman J, Fraile A, García-Mendiola T. Covalent organic polymer-based biosensor for autism spectrum disorder biomarker detection. Mikrochim Acta. 2026; 193(1): 62.

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2. Gultig KD, Boele CP, Roggeveen LEM, Soong TF, Sherry S, Jung C, Milosevska S, Uvarov A, Benhassan K, BenAli SA, Ahajoui Y, Carpio-Arias V, Lindeman S, Koekkoek SKE, Sefik E, Ottenhoff MJ, Wang SS, De Zeeuw CI, El Idrissi A, Boele HJ. Neurobehavioral Assessment of Sensorimotor Function in Autism Using Smartphone Technology. Autism Res. 2026.

Differences in sensorimotor processing represent an important, yet underrecognized, feature of autism; typically assessed through subjective observations, which, although important, are susceptible to biases. To complement these observations, a more objective approach to assess sensorimotor function may be possible through reflex-based neurobehavioral evaluations. The clinical application of these assessments has, however, been largely confined to laboratory settings. Thus, small sample sizes and inconsistent findings have made it challenging to understand how sensorimotor function differs in autism and whether it can be used as an objective biomarker for diagnostics. Here we present a novel smartphone-based platform to conduct neurobehavioral evaluations by measuring facial and behavioral responses in at-home environments. Through a multi-center study, we explored the platform’s ability to distinguish between children with and without autism. We enrolled 536 children aged 3-12 years. BlinkLab smartphone-based assessments were successfully completed in 431 children (80.4%), including 275 with autism and 156 neurotypical children. We found that autistic children showed altered sensorimotor responses across multiple domains. These included reduced prepulse inhibition (PPI), stronger startle habituation over the course of a PPI test, more variable eyeblink responses to auditory stimuli and significant sensitization. Additionally, children with autism displayed more screen avoidance, postural instability, head movements, mouth openings, non-syllabic vocalizations, horizontal pupil shifts, « side-eyeing », and variation in baseline eyelid opening. Exploratory analyses showed that these effects were largely independent of co-occurring conditions. Notably, co-occurrence did influence certain subdomains (e.g., PPI, mouth openings). These findings illustrate that smartphone-based assessments can capture distinct sensorimotor profiles associated with autism in real-world environments. – The way the brain processes sensory information to guide behavior may differ in children with autism. – In this study, we measured sensory processing in autism by looking at facial and postural reactions to ultra‐short sounds while children watched a video, all done on a smartphone. – Autistic children were more startled by these sounds and showed distinct behaviors like mouth openings and vocal sounds that were not commonly seen in neurotypical children. – These findings suggest that differences in sensorimotor processing can be measured with a smartphone application in everyday settings. In the future, these measurements may help us develop new diagnostic tools for autism. eng.

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3. Otkıran G, Erdoğan MA, Uyanıkgil Y, Erbaş O. Prenatal Interferon-Alpha Exposure Induces Autism-Like Neurobehavioral and Neurochemical Alterations in Male Offspring. J Neuroimmune Pharmacol. 2026; 21(1): 4.

Maternal immune activation (MIA) during pregnancy has been implicated as a key environmental risk factor in autism spectrum disorder (ASD). Interferon-alpha (IFN-α), a type I interferon, may disrupt fetal neurodevelopment, yet its mechanistic impact remains insufficiently understood. This study explores the effects of maternal IFN-α exposure on neurobehavioral and neurobiological outcomes in a Wistar rat model. Pregnant rats received IFN-α on gestational day 10, and offspring were evaluated through behavioral assays, neurochemical analyses, and histopathological assessments. IFN-α exposure resulted in significant reductions in GABA, 5-HIAA, and GAD-67 levels, particularly in male offspring, indicating neurotransmitter dysregulation. Histologically, neuronal loss was observed in the hippocampal CA1 and CA3 regions and cerebellar Purkinje cells. Astrocyte activation, reflected by increased GFAP immunoreactivity, was prominent, suggesting a neuroinflammatory response. Additionally, reduced brain-derived neurotrophic factor (BDNF) and elevated tumor necrosis factor-alpha (TNF-α) levels support the presence of inflammation-induced synaptic dysfunction and impaired neuroplasticity. Behaviorally, male offspring exhibited reduced sociability and impaired social novelty recognition. Both sexes demonstrated deficits in motor coordination and exploratory activity. These findings align with core ASD phenotypes and underscore a heightened male vulnerability. Overall, the study provides compelling evidence that prenatal IFN-α exposure leads to persistent neuroimmune, neurochemical, and structural alterations resembling ASD. The results highlight the need for further research into immune-mediated neurodevelopmental disruptions and sex-specific vulnerabilities, offering potential pathways for preventive and therapeutic interventions targeting MIA-related risk mechanisms.

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