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Men and women have always seemed to think in entirely different ways, from conversation and communication to games and gadgets. But are these differences created by society, or do our minds come ready-wired one way or another, with female brains tending towards interaction and male towards organisation? And could this mean that autism rather than being a mental anomaly is in fact simply an extreme male brain? Why are female brains better at empathising? How are male brains designed to analyse systems? And what really makes men and women different? Simon Baron-Cohen explores list-making, lying and two decades of research in a ground-breaking examination of how our brains can be male or female but always completely fascinating

Investigates the differences between the average male & female mind to argue for a mutual respect of difference. The male & female brain types are explained by a dichotomous system of "Empathizing"(E) & "Systematizing"(S). The male & female brains are distinguished by tendencies toward the two characteristics. Analysis of various survey data finds that the female brain is characterized by type E, & the male brain by type S, identifies 5 broad types of brain, & finds that more females than males have an equal S-E balance. A discussion of the extreme Systematizing brain identifies autism as the case of the extreme male brain. Implications of this research to concepts of "gender" question expectations of equal sex ratios in occupations, & the danger of stereotypes and prejudice on the basis of sex. References. J. Harwell

The results leading to this publication have received funding from the Innovative Medicines Initiative 2 Joint Undertaking under grant agreement No 777394 for the project AIMS-2-TRIALS. This Joint Undertaking receives support from the European Union's Horizon 2020 research and innovation programme and EFPIA and AUTISM SPEAKS, Autistica, SFARI. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results. Any views expressed are those of the author(s) and not necessarily those of the funders.

Mindblindness in autism
/ have suggested elsewhere that natural selection had produced a minreading system. In this paper, I will briefly describe four mechanisms which can be considered as four separate components of the human mindreading system : the Intentionality Detector (id), the Eye Direction Detector (edd), the Shared Attention Mechanism (sam) and the Theory-of-Mind Mechanism (tomm). I will report some of the most conclusive experiments which support the view that persons with autism are blind to minds, although id and edd are intact.

To date, neuroimaging research has had a limited focus on non-social features of autism. As a result, neurobiological explanations for atypical sensory perception in autism are lacking. To address this, we quantitively condensed findings from the non-social autism fMRI literature in line with the current best practices for neuroimaging meta-analyses. Using activation likelihood estimation (ALE), we conducted a series of robust meta-analyses across 83 experiments from 52 fMRI studies investigating differences between autistic (n = 891) and typical (n = 967) participants. We found that typical controls, compared to autistic people, show greater activity in the prefrontal cortex (BA9, BA10) during perception tasks. More refined analyses revealed that, when compared to typical controls, autistic people show greater recruitment of the extrastriate V2 cortex (BA18) during visual processing. Taken together, these findings contribute to our understanding of current theories of autistic perception, and highlight some of the challenges of cognitive neuroscience research in autism. ; NJ was supported by the April Trust PhD Studentship awarded by Newnham College. SBC was funded by the Autism Research Trust, the Wellcome Trust, the Templeton World Charitable Foundation, and the NIHR Biomedical Research Centre in Cambridge, during the period of this work. SBC received funding from the Wellcome Trust 214322\Z\18\Z. For the purpose of Open Access, the author has applied a CC BY public copyright licence to any Author Accepted Manuscript version arising from this submission. Further to this SBC received funding from Innovative Medicines Initiative 2 Joint Undertaking (JU) under grant agreement No 777394. The JU receives support from the European Union's Horizon 2020 research and innovation programme and EFPIA and AUTISM SPEAKS, Autistica, SFARI. SBC also received funding from the Autism Research Trust, Autistica, SFARI, the MRC and the NIHR Cambridge Biomedical Research Centre. The research was supported by the National Institute for Health Research (NIHR) Collaboration for Leadership in Applied Health Research and Care East of England at Cambridgeshire and Peterborough NHS Foundation Trust. The views expressed are those of the author(s) and not necessarily those of the NHS, NIHR or Department of Health and Social Care.

Recent research has highlighted a tendency for more rational and deliberative decision-making in individuals with autism. We tested this hypothesis by using eye-tracking to investigate the information processing strategies that underpin multiattribute choice in a sample of adults diagnosed with autism spectrum condition. We found that, as the number of attributes defining each option increased, autistic decision-makers were speedier, examined less of the available information, and spent a greater proportion of their time examining the option they eventually chose. Rather than indicating a more deliberative style, our results are consistent with a tendency for individuals with autism to narrow down the decision-space more quickly than does the neurotypical population. ; This research was funded by a Wellcome Trust (grant RG76641) and Isaac Newton Trust grant (Grant RG70368). GF was also supported by a Wellcome ISSF award (204796/Z/16/Z). PS was supported by the Autism Research Trust and the Wellcome Trust. SBC received funding from the Wellcome Trust 214322/Z/18/Z. In addition, SBC received funding from Innovative Medicines Initiative 2 Joint Undertaking (JU) under grant agreement No 777394. The JU receives support from the European Union's Horizon 2020 research and innovation programme and EFPIA and AUTISM SPEAKS, Autistica, SFARI. SBC also received funding from the Autism Research Trust, SFARI, the Templeton World Charitable Fund, SFARI, and the NIHR Cambridge Biomedical Research Centre. The research was supported by the (U.K.) National Institute for Health Research (NIHR) Collaboration for Leadership in Applied Health Research and Care East of England at Cambridgeshire and Peterborough NHS Foundation Trust.

The Empathizing-Systemizing (E-S) theory of typical sex differences suggests that individuals may be classified based on empathy and systemizing. An extension of the E-S theory, the Extreme Male Brain (EMB) theory suggests that autistic people on average have a shift towards a more masculinized brain along the E-S dimensions. Both theories have been investigated in small sample sizes, limiting their generalizability. Here we leverage two large datasets (discovery n = 671,606, including 36,648 autistic individuals primarily; and validation n = 14,354, including 226 autistic individuals) to investigate 10 predictions of the E-S and the EMB theories. In the discovery dataset, typical females on average showed higher scores on short forms of the Empathy Quotient (EQ) and Sensory Perception Quotient (SPQ), and typical males on average showed higher scores on short forms of the Autism Spectrum Quotient (AQ) and Systemizing Quotient (SQ). Typical sex differences in these measures were attenuated in autistic individuals. Analysis of "brain types" revealed that typical females on average were more likely to be Type E (EQ > SQ) or Extreme Type E and that typical males on average were more likely to be Type S (SQ > EQ) or Extreme Type S. In both datasets, autistic individuals, regardless of their reported sex, on average were "masculinized." Finally, we demonstrate that D-scores (difference between EQ and SQ) account for 19 times more of the variance in autistic traits (43%) than do other demographic variables including sex. Our results provide robust evidence in support of both the E-S and EMB theories. ; This study was supported by the Medical Research Council (MRC), the Wellcome Trust, the Templeton World Charity Foundation, the Autism Research Trust, and the National Institute of Health Research (NIHR) Collaboration for Leadership in Applied Health Research and Care-East of England (CLAHRC-EoE). The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health. The authors also received funding from the Innovative Medicines Initiative 2 Joint Undertaking (JU) under grant agreement No 777394. The JU receives support from the European Union's Horizon 2020 research and innovation programme and EFPIA and Autism Speaks, Autistica, SFARI.

The results leading to this publication have received funding from the Innovative Medicines Initiative 2 Joint Undertaking under grant agreement No 777394 for the project AIMS-2-TRIALS. This Joint Undertaking receives support from the European Union's Horizon 2020 research and innovation programme and EFPIA and AUTISM SPEAKS, Autistica, SFARI. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results. Any views expressed are those of the author(s) and not necessarily those of the funders.

Maternal immune activation (MIA) is mediated by activation of inflammatory pathways resulting in increased levels of cytokines and chemokines that cross the placental and blood-brain barriers altering foetal neural development. Maternal viral infection is one of the most well-known causes for immune activation in pregnant women. MIA and immune abnormalities are key players in the aetiology of developmental conditions such as autism, schizophrenia, ADHD, and depression. Experimental evidence implicating MIA in with different effects in the offspring is complex. For decades, scientists have relied on either MIA models or human epidemiological data or a combination of both. MIA models are generated using infection/pathogenic agents to induce an immunological reaction in rodents and monitor the effects. Human epidemiological studies investigate a link between maternal infection and/or high levels of cytokines in pregnant mothers and the likelihood of developing conditions. In this review, we discuss the importance of understanding the relationship between virus-mediated MIA and neurodevelopmental conditions, focusing on autism and schizophrenia. We further discuss the different methods of studying MIA and their limitations and focus on the different factors contributing to MIA heterogeneity. ; SBC received funding from the Wellcome Trust 214322\Z\18\Z. For the purpose of Open Access, the author has applied a CC BY public copyright licence to any Author Accepted Manuscript version arising from this submission. The results leading to this publication have received funding from the Innovative Medicines Initiative 2 Joint Undertaking under grant agreement No 777394 for the project AIMS-2-TRIALS. This Joint Undertaking receives support from the European Union's Horizon 2020 research and innovation programme and EFPIA and AUTISM SPEAKS, Autistica, SFARI. SBC also received funding from the Autism Centre of Excellence, SFARI, the Templeton World Charitable Fund, the MRC, and the NIHR Cambridge Biomedical Research Centre. ...

The results leading to this publication have received funding from the Innovative Medicines Initiative 2 Joint Undertaking under grant agreement No 777394 for the project AIMS-2-TRIALS. This Joint Undertaking receives support from the European Union's Horizon 2020 research and innovation programme and EFPIA and AUTISM SPEAKS, Autistica, SFARI. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results. Any views expressed are those of the author(s) and not necessarily those of the funders.

The results leading to this publication have received funding from the Innovative Medicines Initiative 2 Joint Undertaking under grant agreement No 777394 for the project AIMS-2-TRIALS. This Joint Undertaking receives support from the European Union's Horizon 2020 research and innovation programme and EFPIA and AUTISM SPEAKS, Autistica, SFARI. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results. Any views expressed are those of the author(s) and not necessarily those of the funders.