Formal Thought Disorder and language impairment in schizophrenia

Radanovic, Márcia; Sousa, Rafael T. de; Valiengo, Leandro; Gattaz, Wagner F.; Forlenza, Orestes Vicente

doi:10.1590/s0004-282x2012005000015

Cited by 30 publications

(16 citation statements)

References 55 publications

(55 reference statements)

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“…Aberrant development of GABAergic interneurons has been linked to several conditions, as autism, epilepsy, Rett syndrome, and schizophrenia (e.g., Di Cristo, 2007). As one may expect given the general cognitive character of these diseases, language is known to be impaired in most of these conditions (Uchino et al, 2001; Veenstra-VanderWeele and Cook, 2004; Tager-Flusberg et al, 2005; Radanovic et al, 2013). If we consider other members of their interactomes (for instance, PTEN, SHH, ELAVL2, FOXG1, etc.)…”

Section: Molecular Basismentioning

confidence: 99%

The shape of the human language-ready brain

2014

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Our core hypothesis is that the emergence of our species-specific language-ready brain ought to be understood in light of the developmental changes expressed at the levels of brain morphology and neural connectivity that occurred in our species after the split from Neanderthals–Denisovans and that gave us a more globular braincase configuration. In addition to changes at the cortical level, we hypothesize that the anatomical shift that led to globularity also entailed significant changes at the subcortical level. We claim that the functional consequences of such changes must also be taken into account to gain a fuller understanding of our linguistic capacity. Here we focus on the thalamus, which we argue is central to language and human cognition, as it modulates fronto-parietal activity. With this new neurobiological perspective in place, we examine its possible molecular basis. We construct a candidate gene set whose members are involved in the development and connectivity of the thalamus, in the evolution of the human head, and are known to give rise to language-associated cognitive disorders. We submit that the new gene candidate set opens up new windows into our understanding of the genetic basis of our linguistic capacity. Thus, our hypothesis aims at generating new testing grounds concerning core aspects of language ontogeny and phylogeny.

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Section: Molecular Basismentioning

confidence: 99%

The shape of the human language-ready brain

2014

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“…Second, schizophrenia has been shown to be implicated in the language and social-modelling areas of the brain. Radanovic et al (2013) discovered a link between formal thought disorder (a diagnostic criterion for schizophrenia) and language impairment. The severity of both impairments was correlated with deficits in the left superior temporal gyrus and the left planum temporale, both areas in a Statistically Standard Brain (SSB) 2 implicated in language; and in the orbitofrontal cortex, which is implicated in modelling for decisionmaking, including social calculus modelling.…”

Section: The Origins Of Self 168mentioning

confidence: 99%

The Origins of Self

2019

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List of figures and tables x Acknowledgements xi Prologue: Down the Rabbit-hole xii ProloguE : Down thE rabbit-holE xiii ProloguE : Down thE rabbit-holE xviii realise, by the end of this book, that there is considerably more down the rabbit-hole than white rabbits: newgenprepdf thE origins of sElf thE origins of sElf 6 thE origins of sElf 12 whErE DiD sElf CoME froM? Large social groups Large brains Joint Enterprise Self-modelling Shared social calculus Intrinsic communication system-LANGUAGE Extrinsic communication system Extrinsic signalling system Relationship-A Social arithmetic

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“…In autism and schizophrenia, theories have posited a "core" dysfunction in social brain [220][221][222][223], in communication [224][225][226] and cognition [227,228]. Such theories have suffered for concentrating on one particular component of human brain evolution, while, in fact, the three components co-evolved and continue to operate in concert.…”

Section: The Hhlrs Problemmentioning

confidence: 99%

Autism and Schizophrenia Are Disorders of Evolvability

Gualtieri¹

2014

OJMP

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Autism and schizophrenia are of particular interest because new developments in genomic medicine address three aspects of the conditions that have been difficult, thus far, to resolve: their heterogeneity, from subclinical manifestations to disorders that are gravely disabling; the genetic basis for their high heritability; and the persistence of disorders in light of their high heritability but low reproductive success they convey. The origins of autism and schizophrenia, their persistence and heterogeneity can be understood by integrating information from genomic science, the social brain and the evolution of socialization, intelligence and language. Both conditions are associated with structural changes in the genome, specifically copy number variants. Such systemic mutations contribute to an unstable and mutable genome and have been especially notable during primate > hominid evolution. Along with mechanisms that affect gene expression, they contribute to a genome characterized by variability and evolvability. A dynamic and variable genome is reflected by a high degree of phenotypic variation. This, in turn, is reflected in the diversity of neurodevelopmental disorders, in particular autism and schizophrenia. Evolvability is more than a dispositional concept, it is a trait in its own right. In the special case of hominid evolution, evolvability has been both an independent and a dependent variable. Evolution of the modern human brain seems to have arisen during the cultivation of unstable regions in the genome that were conducive to a high degree of inter-individual and inter-generational variation. The consequence of even small aberrations in evolutionary processes and phenotypic variations is most likely to be manifest in the functions of the social brain: self-referential processing, perspective taking and the dual components of empathy; also language as well as intelligence itself. The trade-off is a dynamic genome that can rearrange itself in untoward ways and may be felt in one or more of the above functions. The occurrence of neurodevelopmental disorders ranging from the learning disabilities and ADD to autism and schizophrenia, are epiphenomenal to a genome that is unstable and mutable. The selective advantage of such a genome is the runaway evolution of positive prosocial and intellective traits. If there is a core to the pathology that emerges in autism and schizophrenia, it is at the genomic level, and is probably related to the unique evolvability of the human genome. Genetic transformation as an agent of evolvability is necessarily associated with untoward consequences. Just as point mutations may have deleterious effects, so do genomic transformations. The neurodevelopmental disorders, therefore, are the consequence of evolvability.

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Formal Thought Disorder and language impairment in schizophrenia

Cited by 30 publications

References 55 publications

The shape of the human language-ready brain

The shape of the human language-ready brain

The Origins of Self

Autism and Schizophrenia Are Disorders of Evolvability

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