{"doi":"10.3389/fpsyt.2025.1694809","title":"Editorial: Underlying neurobiological, genetic, and behavioral mechanisms in schizophrenia and autism spectrum disorder","abstract":"Understanding potential joint underlying mechanisms of Schizophrenia (SZ) and Autism Spectrum Disorder (AT) is an essential area of study given their phenotypic overlap, including in social communication and social cognition differences1. This research topic sought to invite contributions from researchers to share new scientific evidence on the common and distinct phenotypes and underlying mechanisms between and within SZand AT by employing diverse clinical, behavioral, and neuroscience techniques (e.g., neuroimaging, electrophysiology, genetics, symptom characterization, neurocognitive assessments). The overarching goal of this topic of research is to shed light on the functional significance of symptom profiles and find routes to common new venues for interventions in AT and SZ. The studies shown in this research topic reflect the growth of the current scientific landscape, illustrating the broadening of the standard techniques to new territories and their aim to discover possible common mechanistic pathways. While research directly comparing AT and SZ is not common, few contributions to this topic compared their clinical and cognitive profiles. Nakamura et al. 2 aimed to identify clinical similarities and differences in AT and SZ and proposed a new useful objective predictive model that could aid with differential diagnosis. For that purpose, the authors used a combination of items from assessments validated and typically used in one of the groups only, including the Autism Diagnostic observation Schedule, 2nd edition (ADOS-2) and the Positive and Negative Syndrome Scale (PANSS) to develop a predictive diagnostic model. Their studies revealed that negative symptoms in SZ elevated the ADOS-2 ratings and the ADOS-2 false-positive rates of SZ. Therefore, their proposed predictive model to distinguish SZ and AT included a combination of specific ADOS-2 items (A7, A10, B1, B6, B8, and B9). The study of Nakamura et al., 2 echoed the findings from previous studies by Trevisan et al. 3 and Corbera et al. 4, highlighting the need for better, cross-diagnostic symptom measures for differential diagnosis, given the heterogeneity in clinical presentation of both disorders. Other studies have attempted to examine the shared dysfunctions in these disorders by focusing on neurocognitive profiles instead of symptom profiles. For example, Morais et al.5 examined the executive functioning (EF) profiles in AT, SZ and neurotypical (NT) individuals. Their outcomes showed a substantial overlap in EF deficits with only a few differences in working memory; thus, they suggested tailoring cognitive remediation interventions to these deficits in both populations. While the sample size in this study is relatively small (n=15/group), and results should be replicated, it supports similar interventions for both AT and SZ5. Complementing this, in their review, Guerrera et al.6 advocated for a neurodevelopmental perspective when examining SZ and AT, encouraging the development of large longitudinal studies comparing their phenotypic profile from childhood. Individual studies into disorder-specific mechanisms can also provide valuable insights. For example, the study by Chen et al.7 investigated social-emotional interference in AT children with IQ>80 using an experimental design with modified flanker tasks. Their study provided insightful information about emotional processing in autistic children as they showed that they struggle more than typically developing controls in controlling interference from social information, and that they faced more difficulties as the information load increased, which could hinder their ability to adapt to and engage in social situations. The authors proposed practical, translational strategies offering direct implications for intervention in complex social scenarios such as providing a gradual exposure transition from virtual faces to real faces, and from single faces to different faces. Even though this study focused solely ","journal":"Frontiers in Psychiatry","year":2025,"id":559178,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":1,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9424,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2025-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":1084849,"name":"Rafael Penadés","orcid":"0000-0002-1564-3717","position":1,"is_corresponding":false},{"id":295791,"name":"Michal Assaf","orcid":"0000-0001-5307-1986","position":2,"is_corresponding":false},{"id":466053,"name":"Sílvia Corbera","orcid":"0000-0002-5090-2462","position":0,"is_corresponding":true}],"reference_count":3,"raw_metadata":null,"created_at":"2026-07-19T02:55:34.849815Z","pmid":"41089316","pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}