1. Arthur T, Brosnan M, Harris D, Buckingham G, Wilson M, Williams G, Vine S. Investigating how Explicit Contextual Cues Affect Predictive Sensorimotor Control in Autistic Adults. J Autism Dev Disord;2022 (Sep 5)

Research suggests that sensorimotor difficulties in autism could be reduced by providing individuals with explicit contextual information. To test this, we examined autistic visuomotor control during a virtual racquetball task, in which participants hit normal and unexpectedly-bouncy balls using a handheld controller. The probability of facing each type of ball was varied unpredictably over time. However, during cued trials, participants received explicit information about the likelihood of facing each uncertain outcome. When compared to neurotypical controls, autistic individuals displayed poorer task performance, atypical gaze profiles, and more restricted swing kinematics. These visuomotor patterns were not significantly affected by contextual cues, indicating that autistic people exhibit underlying differences in how prior information and environmental uncertainty are dynamically modulated during movement tasks.

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2. Brosnan M, Ashwin C. Differences in Art Appreciation in Autism: A Measure of Reduced Intuitive Processing. J Autism Dev Disord;2022 (Sep 5)

Art appreciation reflects an initial emotional and intuitive response to artwork evaluation, although this intuitive evaluation can be attenuated by subsequent deliberation. The Dual Process Theory of Autism proposes that individuals with Autism Spectrum Disorder (ASD) have a greater propensity to deliberate and reduced intuition compared to matched controls. Evaluations of high- and low-quality artworks were undertaken by 107 individuals with a diagnosis of ASD and 145 controls. Controls consistently evaluated high-quality artworks to be much better quality than the low-quality artworks, reflecting intuitive processing. The ASD sample showed a reduced difference in evaluations between high- versus low-quality artwork, which reflects reduced intuitive processing and greater deliberative processing and is consistent with predictions by the Dual Process Theory of Autism.

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3. Brynge M, Sjöqvist H, Gardner RM, Lee BK, Dalman C, Karlsson H. Maternal infection during pregnancy and likelihood of autism and intellectual disability in children in Sweden: a negative control and sibling comparison cohort study. Lancet Psychiatry;2022 (Sep 5)

BACKGROUND: Maternal infections during pregnancy are associated with intellectual disability and autism in exposed children. Whether these associations are causal, and therefore should be targets of preventive strategies, remains unknown. We aimed to investigate these associations, to determine whether there is a causal role of maternal infection during pregnancy for children’s risk of autism and intellectual disability, by accounting for unmeasured familial factors. METHODS: We used a register-based cohort study design, and included children living in Stockholm County, Sweden, who were born in 1987-2010. We excluded children not born in Sweden, adopted children, and children with unknown biological mothers or fathers. Maternal infections during pregnancy, defined by ICD-8, ICD-9, and ICD-10 codes, were identified in the National Patient Register and Medical Birth Register. Children were followed up from birth to an outcome or a censoring event (death, migration from Stockholm, age 18 years, or Dec 31, 2016, whichever occurred first). The primary outcomes were diagnosis of autism or diagnosis of intellectual disability. We did a survival analysis to examine the association between inpatient and outpatient specialised care for any infection during pregnancy and likelihood of autism or intellectual disability in the child. To address potential residual confounding, we also estimated the relationship between maternal infection in the year preceding pregnancy as a negative control exposure and conducted a matched sibling analysis of sibling pairs who were discordant for autism or intellectual disability. FINDINGS: 647 947 children living in Stockholm County were identified and, after excluding 97 980 children, we included 549 967 in the study (267 995 [48•7%] were female and 281 972 [51•3%] were male; mean age at censoring 13•5 years [SD 5•0; range <1 to 18]; 142 597 [25•9%] had a mother who was not born in Sweden). 445 (1•3%) of 34 013 children exposed to maternal infection during pregnancy were diagnosed with intellectual disability and 1123 (3•3%) with autism. 5087 (1•0%) of 515 954 unexposed children were diagnosed with intellectual disability and 13 035 (2•5%) with autism. Maternal infection during pregnancy was associated with autism (hazard ratio [HR] 1•16, 95% CI 1•09-1•23) and intellectual disability (1•37, 1•23-1•51) in exposed children compared with unexposed children. Maternal infection in the year before pregnancy (negative control exposure) was also associated with autism (HR 1•25, 95% CI 1•14-1•36), but was not associated with intellectual disability (1•09, 0•94-1•27). In sibling comparisons, the associations with maternal infection during pregnancy were attenuated for autism (HR 0•94, 95% CI 0•82-1•08; n=21 864), but not to the same extent for intellectual disability (1•15, 0•95-1•40; n=9275). INTERPRETATION: Although infections in pregnant women are associated with both autism and intellectual disability in their children, the association with autism does not appear to reflect a causal relationship, but is more likely to be explained by factors shared between family members such as genetic variation or aspects of the shared environment. Thus, infection prevention is not expected to reduce autism incidence. For intellectual disability, unmeasured familial factors might not fully explain the observed associations, and a causal role of maternal infections cannot be excluded. Causal effects of specific but rare infections or infections not requiring health care contact cannot be excluded in either autism or intellectual disability. FUNDING: Swedish Research Council, Stanley Medical Research Institute, and Autism Speaks. TRANSLATION: For the Swedish translation of the abstract see Supplementary Materials section.

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4. Chen YC, Lin HY, Chien Y, Tung YH, Ni YH, Gau SS. Altered gut microbiota correlates with behavioral problems but not gastrointestinal symptoms in individuals with autism. Brain Behav Immun;2022 (Sep 2);106:161-178.

BACKGROUND: Despite inconsistent results across studies, emerging evidence suggests that the microbial micro-environment may be associated with autism spectrum disorder (ASD). Geographical and cultural factors highly impact microbial profiles, and there is a shortage of data from East Asian populations. This study aimed to comprehensively characterize microbial profiles in an East Asian sample and explore whether gut microbiota contributes to clinical symptoms, emotional/behavioral problems, and GI symptoms in ASD. METHODS: We assessed 82 boys and young men with ASD and 31 typically developing controls (TDC), aged 6-25 years. We analyzed the stool sample of all participants with 16S V3-V4 rRNA sequencing and correlated its profile with GI symptoms, autistic symptoms, and emotional/behavioral problems. RESULTS: Autistic individuals, compared to TDC, had worse GI symptoms. There were no group differences in alpha diversity of species richness estimates (Shannon-wiener and Simpson diversity indices). Participants with ASD had an increased relative abundance of Fusobacterium, Ruminococcus torques group (at the genus level), and Bacteroides plebeius DSM 17135 (at the species level), while a decreased relative abundance of Ruminococcaceae UCG 013, Ervsipelotrichaceae UCG 003, Parasutterella, Clostridium sensu stricto 1, Turicibacter (at the genus level), and Clostridium spiroforme DSM 1552 and Intestinimonas butyriciproducens (at the species level). Altered taxonomic diversity in ASD significantly correlated with autistic symptoms, thought problems, delinquent behaviors, self dysregulation, and somatic complaints. We did not find an association between gut symptoms and gut microbial dysbiosis. CONCLUSIONS: Our findings suggest that altered microbiota are associated with behavioral phenotypes but not GI symptoms in ASD. The function of the identified microbial profiles mainly involves the immune pathway, supporting the hypothesis of a complex relationship between altered microbiome, immune dysregulation, and ASD that may advance the discovery of molecular biomarkers for ASD.

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5. Kaiser FMP, Gruenbacher S, Oyaga MR, Nio E, Jaritz M, Sun Q, van der Zwaag W, Kreidl E, Zopf LM, Dalm V, Pel J, Gaiser C, van der Vliet R, Wahl L, Rietman A, Hill L, Leca I, Driessen G, Laffeber C, Brooks A, Katsikis PD, Lebbink JHG, Tachibana K, van der Burg M, De Zeeuw CI, Badura A, Busslinger M. Biallelic PAX5 mutations cause hypogammaglobulinemia, sensorimotor deficits, and autism spectrum disorder. J Exp Med;2022 (Sep 5);219(9)

The genetic causes of primary antibody deficiencies and autism spectrum disorder (ASD) are largely unknown. Here, we report a patient with hypogammaglobulinemia and ASD who carries biallelic mutations in the transcription factor PAX5. A patient-specific Pax5 mutant mouse revealed an early B cell developmental block and impaired immune responses as the cause of hypogammaglobulinemia. Pax5 mutant mice displayed behavioral deficits in all ASD domains. The patient and the mouse model showed aberrant cerebellar foliation and severely impaired sensorimotor learning. PAX5 deficiency also caused profound hypoplasia of the substantia nigra and ventral tegmental area due to loss of GABAergic neurons, thus affecting two midbrain hubs, controlling motor function and reward processing, respectively. Heterozygous Pax5 mutant mice exhibited similar anatomic and behavioral abnormalities. Lineage tracing identified Pax5 as a crucial regulator of cerebellar morphogenesis and midbrain GABAergic neurogenesis. These findings reveal new roles of Pax5 in brain development and unravel the underlying mechanism of a novel immunological and neurodevelopmental syndrome.

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6. Korisky A, Gordon I, Goldstein A. Oxytocin impacts top-down and bottom-up social perception in adolescents with ASD: a MEG study of neural connectivity. Mol Autism;2022 (Sep 5);13(1):36.

BACKGROUND: In the last decade, accumulative evidence has shown that oxytocin can modulate social perception in typically developed individuals and individuals diagnosed with autism. While several studies show that oxytocin (OT) modulates neural activation in social-related neural regions, the mechanism that underlies OT effects in ASD is not fully known yet. Despite evidence from animal studies on connections between the oxytocinergic system and excitation/inhibition neural balance, the influence of OT on oscillatory responses among individuals with ASD has been rarely examined. To bridge these gaps in knowledge, we investigated the effects of OT on both social and non-social stimuli while focusing on its specific influence on the neural connectivity between three socially related neural regions-the left and right fusiform and the medial frontal cortex. METHODS: Twenty-five adolescents with ASD participated in a wall-established social task during a randomized, double-blind placebo-controlled MEG and OT administration study. Our main task was a social-related task that required the identification of social and non-social-related pictures. We hypothesized that OT would modulate the oscillatory connectivity between three pre-selected regions of interest to be more adaptive to social processing. Specifically, we focused on alpha and gamma bands which are known to play an important role in face processing and top-down/bottom-up balance. RESULTS: Compared to placebo, OT reduced the connectivity between the medial frontal cortex and the fusiform in the low gamma more for social stimuli than for non-social ones, a reduction that was correlated with individuals’ performance in the task. Additionally, for both social and non-social stimuli, OT increased the connectivity in the alpha and beta bands. LIMITATIONS: Sample size was determined based on sample sizes previously reported in MEG in clinical populations, especially OT administration studies in combination with neuroimaging in ASD. We were limited in our capability to recruit for such a study, and as such, the sample size was not based on a priori power analysis. Additionally, we limited our analyses to specific neural bands and regions. To validate the current results, future studies may be needed to explore other parameters using whole-brain approaches in larger samples. CONCLUSION: These results suggest that OT influenced social perception by modifying the communication between frontal and posterior regions, an attenuation that potentially impacts both social and non-social early perception. We also show that OT influences differ between top-down and bottom-up processes, depending on the social context. Overall, by showing that OT influences both social-related perception and overall attention during early processing stages, we add new information to the existing understanding of the impact of OT on neural processing in ASD. Furthermore, by highlighting the influence of OT on early perception, we provide new directions for treatments for difficulties in early attentional phases in this population. Trial registration Registered on October 27, 2021-Retrospectively registered, https://clinicaltrials.gov/ct2/show/record/NCT05096676 (details on clinical registration can be found in www. CLINICALTRIAL: gov , unique identifier: NCT05096676 ).

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7. Mei T, Forde NJ, Floris DL, Dell’Acqua F, Stones R, Ilioska I, Durston S, Moessnang C, Banaschewski T, Holt RJ, Baron-Cohen S, Rausch A, Loth E, Oakley B, Charman T, Ecker C, Murphy DGM, Beckmann CF, Llera A, Buitelaar JK. Autism is associated with inter-individual variations of gray and white matter morphology. Biol Psychiatry Cogn Neurosci Neuroimaging;2022 (Sep 5)

BACKGROUND: Although many studies have explored atypicalities in gray and white matter (GM, WM) morphology of autism, most of them rely on unimodal analyses that do not benefit from the likelihood that different imaging modalities may reflect common neurobiology. We aimed to establish brain patterns of modalities that differentiate between autism and controls and explore associations between these brain patterns and clinical measures. METHODS: We studied 183 individuals with autism and 157 non-autistic individuals (6-30 years) in a large deeply phenotyped autism dataset (EU-AIMS LEAP). Linked Independent Component Analysis was utilized to link all participants’ GM volume and WM diffusion tensor images, and group comparisons of modality shared variances were examined. Subsequently, we performed univariate and multivariate brain-behavior correlation analyses to separately explore the relations between brain patterns and clinical profiles. RESULTS: One multimodal pattern was significantly related to autism. This pattern was primarily associated with GM volume in bilateral insula, frontal, pre- and post-central, cingulate, and caudate areas, and co-occurred with altered WM features in the superior longitudinal fasciculus. The brain-behavior correlation analyses showed a significant multivariate association primarily between brain patterns that involved variation of WM, and symptoms of restricted and repetitive behavior in the autism group. CONCLUSIONS: Our findings demonstrate the assets of integrated analyses of GM and WM alterations to study the brain mechanisms that underpin autism, and show that the complex clinical autism phenotype can be interpreted by brain covariation patterns that are spread across the brain involving both cortical and subcortical areas.

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8. Mohammadkhani R, Ghahremani R, Salehi I, Safari S, Karimi SA, Zarei M. Impairment in social interaction and hippocampal long-term potentiation at perforant pathway-dentate gyrus synapses in a prenatal valproic acid-induced rat model of autism. Brain Commun;2022;4(5):fcac221.

It is well established that prenatal valproic acid exposure in rats leads to autism-like behaviours and social deficits. Long-term potentiation changes in the brain have been proposed as a potential mechanism in the development of autistic behaviour. However, there are controversies regarding the effect of in utero valproic acid exposure on long-term potentiation. This study examined the social interaction and long-term potentiation induction in perforant pathway-dentate gyrus synapses in male offspring of a rat model of autism induced by prenatal exposure to valproic acid. On Embryonic Day 12.5, the pregnant dams received an injection of 500 mg/kg valproic acid (intraperitoneal) to produce the autism model. The sociability test was performed between Postnatal Days 37 and 40. The offsprings were urethane-anaesthetized and placed into a stereotaxic apparatus for surgery, electrode implantation and field potential recording on Postnatal Days 45-55. In the dentate gyrus region, excitatory postsynaptic potential slope and population spike amplitude were measured. Valproic acid-exposed offspring showed significantly impaired social interaction. The birth weight in valproic acid-exposed rats was significantly lower than in control rats. The ability of dentate gyrus synapses to induce long-term potentiation was hampered by valproic acid exposure. The decreasing excitatory postsynaptic potential slope and population spike amplitude of long-term potentiation provide evidence in favour of this notion. It is widely supposed that the hippocampus plays a central role in the process of learning and memory as well as social interaction and social memory. Therefore, deficiencies in hippocampal synaptic plasticity may be responsible, at least in part, for the social interaction deficits in valproic acid-exposed rats.

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9. Pellicano E, Fatima U, Hall G, Heyworth M, Lawson W, Lilley R, Mahony J, Stears M. A capabilities approach to understanding and supporting autistic adulthood. Nat Rev Psychol;2022 (Sep 5):1-16.

There is little comprehensive research into autistic adulthood, and even less into the services and supports that are most likely to foster flourishing adult autistic lives. This limited research is partly because autism is largely conceived as a condition of childhood, but this focus of research has also resulted from the orthodox scientific approach to autism, which conceptualizes autistic experience almost entirely as a series of biologically derived functional deficits. Approaching autism in this way severely limits what is known about this neurodevelopmental difference, how research is conducted and the services and supports available. In this Review, we adopt an alternative research strategy: we apply Martha Nussbaum’s capabilities approach, which focuses on ten core elements of a thriving human life, to research on autistic adulthood. In doing so, we identify areas where autistic adults thrive and where they often struggle, and highlight issues to which researchers, clinicians and policymakers should respond. The resulting picture is far more complex than conventional accounts of autism imply. It also reveals the importance of engaging autistic adults directly in the research process to make progress towards genuinely knowing autism and supporting flourishing autistic lives.

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10. Purushotham SS, Reddy NMN, D’Souza MN, Choudhury NR, Ganguly A, Gopalakrishna N, Muddashetty R, Clement JP. A perspective on molecular signalling dysfunction, its clinical relevance and therapeutics in autism spectrum disorder. Exp Brain Res;2022 (Sep 5)

Intellectual disability (ID) and autism spectrum disorder (ASD) are neurodevelopmental disorders that have become a primary clinical and social concern, with a prevalence of 2-3% in the population. Neuronal function and behaviour undergo significant malleability during the critical period of development that is found to be impaired in ID/ASD. Human genome sequencing studies have revealed many genetic variations associated with ASD/ID that are further verified by many approaches, including many mouse and other models. These models have facilitated the identification of fundamental mechanisms underlying the pathogenesis of ASD/ID, and several studies have proposed converging molecular pathways in ASD/ID. However, linking the mechanisms of the pathogenic genes and their molecular characteristics that lead to ID/ASD has progressed slowly, hampering the development of potential therapeutic strategies. This review discusses the possibility of recognising the common molecular causes for most ASD/ID based on studies from the available models that may enable a better therapeutic strategy to treat ID/ASD. We also reviewed the potential biomarkers to detect ASD/ID at early stages that may aid in diagnosis and initiating medical treatment, the concerns with drug failure in clinical trials, and developing therapeutic strategies that can be applied beyond a particular mutation associated with ASD/ID.

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11. Shahrudin FA, Dzulkarnain AAA, Hanafi AM, Jamal FN, Basri NA, Sidek SN, Yusof HM, Khalid M. Music and Sound-Based Intervention in Autism Spectrum Disorder: A Scoping Review. Psychiatry Investig;2022 (Aug);19(8):626-636.

To map the evidence from the relevant studies regarding the use of music and sound-based intervention for autism spectrum disorder (ASD) using a scoping review study design. Scoping review was conducted according to the inclusion criteria using Google Scholar, PubMed, CINAHL, MEDLINE, and Scopus. The review was accomplished in five steps: 1) identify the inclusion criteria, 2) search for relevant studies, 3) studies selection, 4) data extraction and charting, and 5) data analysis and presentation. Four major themes emerged from 39 studies that matched the inclusion criteria as follows: 1) forms of sound therapy discussing methods of sound therapy and stimulus used, 2) duration of the intervention explain in terms of listening time and total listening sessions, 3) clinical characteristics of the intervention exploring the main interest of sound therapy study in ASD, and 4) evidence for the intervention effectiveness looking into the positive, negative, and mixed findings of previous studies. Each theme was explored to identify the knowledge gaps in sound-intervention therapy. This review demonstrated the need for further studies to address several issues including identifying the effectiveness of sound-therapy intervention for ASD according to the individual sound types, the minimum duration for ASD sound-therapy intervention and more details on the use of technology, and clinical features of the sound-therapy intervention. These elements are important to further demonstrate the effectiveness of sound therapy intervention for ASD children.

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12. Yon-Hernández JA, Wojcik DZ, García-García L, Magán-Maganto M, Franco-Martín M, Canal-Bedia R. Neuropsychological profile of executive functions in autism spectrum disorder and schizophrenia spectrum disorders: a comparative group study in adults. Eur Arch Psychiatry Clin Neurosci;2022 (Sep 5)

As assessed by numerous neuropsychological tasks, individuals with autism spectrum disorder (ASD) and schizophrenia spectrum disorders (SSDs) have similar impairments related to executive functions (EFs). The neuropsychological profile of these two conditions was examined using the three-component EFs’ framework of Miyake and Friedman (Cogn Psychol 41(1):49-100, 2000). This approach assesses Inhibition (suppression of unwanted and irrelevant information/responses), Updating (use and control of contents of working memory), and Shifting (disengagement between activities or mental tasks) using nine different tasks. In line with previous research, we expected greater performance deficits in ASD in all three components compared to SSD, as well as faster responses for the SSD group. A self-paced task format allowed us to examine whether unlimited time given for a task would lead to better performance. The sample was constituted by the control group (N = 25), ASD group (N = 24), and SSD group (N = 12). Groups did not differ on Inhibition performance. In Updating, individuals with SSD performed poorer than the other groups. As for Shifting, both groups demonstrated poorer performance compared to controls, with the SSD group presenting the greatest difficulties. In terms of reaction time (RT), SSD participants’ RT were the slowest on Inhibition and Shifting tasks. There was a positive correlation between performance and time spent on Inhibition and Shifting only for the SSD group, which demonstrates that their performance improves when there are no time constraints. Our work provides a better understanding of spared and impaired EFs, which could be useful for designing strategies aimed at improving specific EFs in each group.

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13. Yue Y, Ash RT, Boyle N, Kinter A, Li Y, Zeng C, Lu H. MeCP2 deficiency impairs motor cortical circuit flexibility associated with motor learning. Mol Brain;2022 (Sep 5);15(1):76.

Loss of function mutations in the X-linked gene encoding methyl-CpG binding protein 2 (MECP2) cause Rett syndrome (RTT), a postnatal neurological disorder. The loss of motor function is an important clinical feature of RTT that manifests early during the course of the disease. RTT mouse models with mutations in the murine orthologous Mecp2 gene replicate many human phenotypes, including progressive motor impairments. However, relatively little is known about the changes in circuit function during the progression of motor deficit in this model. As the motor cortex is the key node in the motor system for the control of voluntary movement, we measured firing activity in populations of motor cortical neurons during locomotion on a motorized wheel-treadmill. Different populations of neurons intermingled in the motor cortex signal different aspects of the locomotor state of the animal. The proportion of running selective neurons whose activity positively correlates with locomotion speed gradually decreases with weekly training in wild-type mice, but not in Mecp2-null mice. The fraction of rest-selective neurons whose activity negatively correlates with locomotion speed does not change with training in wild-type mice, but is higher and increases with the progression of locomotion deficit in mutant mice. The synchronization of population activity that occurs in WT mice with training did not occur in Mecp2-null mice, a phenotype most clear during locomotion and observable across all functional cell types. Our results could represent circuit-level biomarkers for motor regression in Rett syndrome.

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14. Zhang Y, Pang Y, Feng W, Jin Y, Chen S, Ding S, Wang Z, Zou Y, Li Y, Wang T, Sun P, Gao J, Zhu Y, Ke X, Marshall C, Huang H, Sheng C, Xiao M. miR-124 regulates early isolation-induced social abnormalities via inhibiting myelinogenesis in the medial prefrontal cortex. Cell Mol Life Sci;2022 (Sep 4);79(9):507.

Patients with autism spectrum disorder (ASD) typically experience substantial social isolation, which may cause secondary adverse effects on their brain development. miR-124 is the most abundant miRNA in the human brain, acting as a pivotal molecule regulating neuronal fate determination. Alterations of miR-124 maturation or expression are observed in various neurodevelopmental, neuropsychiatric, and neurodegenerative disorders. In the present study, we analyzed a panel of brain-enriched microRNAs in serums from 2 to 6 year old boys diagnosed with ASD. The hsa-miR-124 level was found significantly elevated in ASD boys than in age and sex-matched healthy controls. In an isolation-reared weanling mouse model, we evidenced elevated mmu-miR-124 level in the serum and the medial prefrontal cortex (mPFC). These mice displayed significant sociability deficits, as well as myelin abnormality in the mPFC, which was partially rescued by expressing the miR-124 sponge in the bilateral mPFC, ubiquitously or specifically in oligodendroglia. In cultured mouse oligodendrocyte precursor cells, introducing a synthetic mmu-miR-124 inhibited the differentiation process through suppressing expression of nuclear receptor subfamily 4 group A member 1 (Nr4a1). Overexpressing Nr4a1 in the bilateral mPFC also corrected the social behavioral deficits and myelin impairments in the isolation-reared mice. This study revealed an unanticipated role of the miR-124/Nr4a1 signaling in regulating early social experience-dependent mPFC myelination, which may serve as a potential therapy target for social neglect or social isolation-related neuropsychiatric disorders.

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