The Evolutionary Biology of Human Neurodevelopment

Crespi, Bernard J.; Leach, Emma

doi:10.1002/9781118524756.ch9

Cited by 20 publications

(4 citation statements)

References 119 publications

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“…A recent study found a nominal association of DAOA rs3916971 with a psychotic disorder ( 57 ). Another study conducted in healthy male controls found that DAOA rs3916971 schizophrenia risk C-allele carriers had worse visual-spatial skills ( 58 , 59 ). In our study, DAO rs3918347 GA + AA genotype carriers experienced nominally more auditory perception disturbances than GG genotype carriers at baseline (RDoC cognitive system).…”

Section: Discussionmentioning

confidence: 99%

Prediction Analysis for Transition to Schizophrenia in Individuals at Clinical High Risk for Psychosis: The Relationship of DAO, DAOA, and NRG1 Variants with Negative Symptoms and Cognitive Deficits

et al. 2017

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Schizophrenia is characterized by positive and negative symptoms and cognitive dysfunction. The glutamate hypothesis of schizophrenia has been hypothesized to explain the negative symptoms and cognitive deficits better than the dopamine hypothesis alone. Therefore, we aimed to evaluate whether glutamatergic variants such as d-amino acid oxidase (DAO), DAO activator (DAOA)/G72, and neuregulin 1 (NRG1) single-nucleotide polymorphisms (SNPs) and their mRNA levels predicted (i) transition to schizophrenia spectrum disorders and (ii) research domain criteria (RDoC) domains, mainly negative valence and cognitive systems. In a 3-year prospective study cohort of 185 individuals (age: 13–35 years) at high risk and ultra-high risk (UHR) for psychosis, we assessed DAO (rs3918347, rs4623951), DAOA (rs778293, rs3916971, rs746187), and NRG1 (rs10503929) SNPs and their mRNA expression. Furthermore, we investigated their association with RDoC domains, mainly negative valence (e.g., anxiety, hopelessness) and cognitive (e.g., perception disturbances, disorganized symptoms) systems. NRG1 rs10503929 CC + CT versus TT genotype carriers experienced significantly more disorganized symptoms. DAOA rs746187 CC versus CT + TT genotype, DAOA rs3916971 TT versus TC + CC genotype, and DAO rs3918347 GA + AA versus GG genotype carriers experienced nominally more hopelessness, visual perception disturbances, and auditory perception disturbances, respectively. The schizophrenia risk G-allele of DAO rs3918347 nominally increased risk for those UHR individuals with attenuated positive symptoms syndrome. No association between DAO, DAOA, NRG1 SNPs, and conversion to schizophrenia spectrum disorders was observed. Our findings suggest that DAO, DAOA, and NRG1 polymorphisms might influence both RDoC negative valence and cognitive systems, but not transition to schizophrenia spectrum disorders.

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Section: Discussionmentioning

confidence: 99%

Prediction Analysis for Transition to Schizophrenia in Individuals at Clinical High Risk for Psychosis: The Relationship of DAO, DAOA, and NRG1 Variants with Negative Symptoms and Cognitive Deficits

et al. 2017

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“…Finally, autism is the only psychiatric condition characterized by notable rates of savant skills, which in this context represent highly-structured, rule-based abilities largely restricted to a few spheres of mental ability: calendar calculating, rote memory, mathematical computation, musical memory, and realistic drawing (Howlin et al, 2009 ; Snyder, 2009 ; Treffert, 2014 ; Meilleur et al, 2015 ). Savantism appears to represent an extreme of imbalanced components of mental ability in autism, given its highly limited range of enhancements and apparent negative associations of special skills with verbal and social abilities (Crespi and Leach, 2016 ).…”

Section: Autism and The Correlates Of Intelligencementioning

confidence: 99%

“…Risks for autism, like risks of cancer, diabetes, or arthritis, have evolved along the human lineage (Crespi and Leach, 2016 ). As such, evolutionary biology becomes a valuable conceptual and analytic tool for connecting adaptive brain systems with the ways in which they can become altered and maladaptive in psychiatric disorders (Fjell et al, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

Autism As a Disorder of High Intelligence

Crespi

2016

Front. Neurosci.

127

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A suite of recent studies has reported positive genetic correlations between autism risk and measures of mental ability. These findings indicate that alleles for autism overlap broadly with alleles for high intelligence, which appears paradoxical given that autism is characterized, overall, by below-average IQ. This paradox can be resolved under the hypothesis that autism etiology commonly involves enhanced, but imbalanced, components of intelligence. This hypothesis is supported by convergent evidence showing that autism and high IQ share a diverse set of convergent correlates, including large brain size, fast brain growth, increased sensory and visual-spatial abilities, enhanced synaptic functions, increased attentional focus, high socioeconomic status, more deliberative decision-making, profession and occupational interests in engineering and physical sciences, and high levels of positive assortative mating. These findings help to provide an evolutionary basis to understanding autism risk as underlain in part by dysregulation of intelligence, a core human-specific adaptation. In turn, integration of studies on intelligence with studies of autism should provide novel insights into the neurological and genetic causes of high mental abilities, with important implications for cognitive enhancement, artificial intelligence, the relationship of autism with schizophrenia, and the treatment of both autism and intellectual disability.

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“…The roles of testosterone and oxytocin in other psychiatric disorders involving dysregulated social cognition, especially the major psychotic-affective disorders schizophrenia, bipolar disorder, and depression that share symptoms and risk factors, have been less well investigated than for autism, both theoretically and empirically; indeed, conceptual, hypothetic-deductive frameworks have yet to be developed in this context, despite the obvious importance of social hormones in human psychological phenotypes. A recently developed model for understanding the psychotic-affective disorders, in comparison to autism, is that they involve forms of dysfunctional, 'hyper-developed' social cognition, as demonstrated, for example, in such phenotypes as paranoia, other social delusions, auditory hallucination, megalomania, high levels of social emotion including guilt, shame, pride, or embarrassment, high empathic drive, and high social motivation as observed in mania (Crespi & Badcock, 2008;Backasch et al, 2013;Sharp et al, 2013;Crespi & Leach, 2015). This model is based on the simple presumptions that evolution along the human lineage has predominantly involved increases in social cognition and emotionality (the well-supported 'social brain' hypothesis) (Dunbar & Shultz, 2007), and that all biological phenotypes can be perturbed in two opposite directions, towards either lower or higher expression of some trait, pathway, or system, both of which cause performance deficits although by different means.…”

Section: ) Oxytocin and Testosterone In Psychotic-affective Conditionsmentioning

confidence: 99%

Oxytocin, testosterone, and human social cognition

2015

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I describe an integrative social-evolutionary model for the adaptive significance of the human oxytocinergic system. The model is based on a role for this hormone in the generation and maintenance of social familiarity and affiliation across five homologous, functionally similar, and sequentially co-opted contexts: mothers with offspring, female and male mates, kin groups, individuals with reciprocity partners, and individuals within cooperating and competing social groups defined by culture. In each situation, oxytocin motivates, mediates and rewards the cognitive and behavioural processes that underlie the formation and dynamics of a more or less stable social group, and promotes a relationship between two or more individuals. Such relationships may be positive (eliciting neurological reward, reducing anxiety and thus indicating fitness-enhancing effects), or negative (increasing anxiety and distress, and thus motivating attempts to alleviate a problematic, fitness-reducing social situation). I also present evidence that testosterone exhibits opposite effects from oxytocin on diverse aspects of cognition and behaviour, most generally by favouring self-oriented, asocial and antisocial behaviours. I apply this model for effects of oxytocin and testosterone to understanding human psychological disorders centrally involving social behaviour. Reduced oxytocin and higher testosterone levels have been associated with under-developed social cognition, especially in autism. By contrast, some combination of oxytocin increased above normal levels, and lower testosterone, has been reported in a notable number of studies of schizophrenia, bipolar disorder and depression, and, in some cases, higher oxytocin involves maladaptively 'hyper-developed' social cognition in these conditions. This pattern of findings suggests that human social cognition and behaviour are structured, in part, by joint and opposing effects of oxytocin and testosterone, and that extremes of such joint effects partially mediate risks and phenotypes of autism and psychotic-affective conditions. These considerations have direct implications for the development of therapies for alleviating disorders of social cognition, and for understanding how such disorders are associated with the evolution of human cognitive-affective architecture.

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The Evolutionary Biology of Human Neurodevelopment

Cited by 20 publications

References 119 publications

Prediction Analysis for Transition to Schizophrenia in Individuals at Clinical High Risk for Psychosis: The Relationship of DAO, DAOA, and NRG1 Variants with Negative Symptoms and Cognitive Deficits

Prediction Analysis for Transition to Schizophrenia in Individuals at Clinical High Risk for Psychosis: The Relationship of DAO, DAOA, and NRG1 Variants with Negative Symptoms and Cognitive Deficits

Autism As a Disorder of High Intelligence

Oxytocin, testosterone, and human social cognition

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