Antonio Benítez-Burraco

The shape of the human language-ready brain.

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.

Globularity and language-readiness: generating new predictions by expanding the set of genes of interest

This study builds on the hypothesis put forth in Boeckx and Benítez-Burraco (2014), according to which the developmental changes expressed at the levels of brain morphology and neural connectivity that resulted in a more globular braincase in our species were crucial to understand the origins of our language-ready brain. Specifically, this paper explores the links between two well-known ‘language-related’ genes like FOXP2 and ROBO1 implicated in vocal learning and the initial set of genes of interest put forth in Boeckx and Benítez-Burraco (2014), with RUNX2 as focal point. Relying on the existing literature, we uncover potential molecular links that could be of interest to future experimental inquiries into the biological foundations of language and the testing of our initial hypothesis. Our discussion could also be relevant for clinical linguistics and for the interpretation of results from paleogenomics.

Possible functional links among brain- and skull-related genes selected in modern humans

The sequencing of the genomes from extinct hominins has revealed that changes in some brain-related genes have been selected after the split between anatomically-modern humans and Neanderthals/Denisovans. To date, no coherent view of these changes has been provided. Following a line of research we initiated in Boeckx and Benítez-Burraco (2014a), we hypothesize functional links among most of these genes and their products, based on the existing literature for each of the gene discussed. The genes we focus on are found mutated in different cognitive disorders affecting modern populations and their products are involved in skull and brain morphology, and neural connectivity. If our hypothesis turns out to be on the right track, it means that the changes affecting most of these proteins resulted in a more globular brain and ultimately brought about modern cognition, with its characteristic generativity and capacity to form and exploit cross-modular concepts, properties most clearly manifested in language.

Universal Grammar and Biological Variation: An EvoDevo Agenda for Comparative Biolinguistics

Recent advances in genetics and neurobiology have greatly increased the degree of variation that one finds in what is taken to provide the biological foundations of our species-specific linguistic capacities. In particular, this variation seems to cast doubt on the purportedly homogeneous nature of the language faculty traditionally captured by the concept of “Universal Grammar.” In this article we discuss what this new source of diversity reveals about the biological reality underlying Universal Grammar. Our discussion leads us to support (1) certain hypotheses advanced in evolutionary developmental biology that argue for the existence of robust biological mechanisms capable of canalizing variation at different levels, and (2) a bottom-up perspective on comparative cognition. We conclude by sketching future directions for what we call “comparative biolinguistics,” specifying which experimental directions may help us succeed in this new research avenue.

The archaeological record speaks: bridging anthropology and linguistics.

This paper examines the origins of language, as treated within Evolutionary Anthropology, under the light offered by a biolinguistic approach. This perspective is presented first. Next we discuss how genetic, anatomical, and archaeological data, which are traditionally taken as evidence for the presence of language, are circumstantial as such from this perspective. We conclude by discussing ways in which to address these central issues, in an attempt to develop a collaborative approach to them.

The Oscillopathic Nature of Language Deficits in Autism: From Genes to Language Evolution

Autism spectrum disorders (ASD) are pervasive neurodevelopmental disorders involving a number of deficits to linguistic cognition. The gap between genetics and the pathophysiology of ASD remains open, in particular regarding its distinctive linguistic profile. The goal of this article is to attempt to bridge this gap, focusing on how the autistic brain processes language, particularly through the perspective of brain rhythms. Due to the phenomenon of pleiotropy, which may take some decades to overcome, we believe that studies of brain rhythms, which are not faced with problems of this scale, may constitute a more tractable route to interpreting language deficits in ASD and eventually other neurocognitive disorders. Building on recent attempts to link neural oscillations to certain computational primitives of language, we show that interpreting language deficits in ASD as oscillopathic traits is a potentially fruitful way to construct successful endophenotypes of this condition. Additionally, we will show that candidate genes for ASD are overrepresented among the genes that played a role in the evolution of language. These genes include (and are related to) genes involved in brain rhythmicity. We hope that the type of steps taken here will additionally lead to a better understanding of the comorbidity, heterogeneity, and variability of ASD, and may help achieve a better treatment of the affected populations.

Language deficits in schizophrenia and autism as related oscillatory connectomopathies: An evolutionary account

HighlightsSZ and ASD display markedly similar oscillatory profiles with respect to their linguistic deficits.These ‘oscillopathies’ are used to inform debates about dynamic language processing in the brain.Candidate genes for SZ and ASD are overrepresented among the gene sets believed to be important for language evolution. Abstract Schizophrenia (SZ) and autism spectrum disorders (ASD) are characterised by marked language deficits, but it is not clear how these arise from gene mutations associated with the disorders. Our goal is to narrow the gap between SZ and ASD and, ultimately, give support to the view that they represent abnormal (but related) ontogenetic itineraries for the human faculty of language. We will focus on the distinctive oscillatory profiles of the SZ and ASD brains, in turn using these insights to refine our understanding of how the brain implements linguistic computations by exploring a novel model of linguistic feature‐set composition. We will argue that brain rhythms constitute the best route to interpreting language deficits in both conditions and mapping them to neural dysfunction and risk alleles of the genes. Importantly, candidate genes for SZ and ASD are overrepresented among the gene sets believed to be important for language evolution. This translational effort may help develop an understanding of the aetiology of SZ and ASD and their high prevalence among modern populations.

Bridging the Gap between Genes and Language Deficits in Schizophrenia: An Oscillopathic Approach

Schizophrenia is characterized by marked language deficits, but it is not clear how these deficits arise from the alteration of genes related to the disease. The goal of this paper is to aid the bridging of the gap between genes and schizophrenia and, ultimately, give support to the view that the abnormal presentation of language in this condition is heavily rooted in the evolutionary processes that brought about modern language. To that end we will focus on how the schizophrenic brain processes language and, particularly, on its distinctive oscillatory profile during language processing. Additionally, we will show that candidate genes for schizophrenia are overrepresented among the set of genes that are believed to be important for the evolution of the human faculty of language. These genes crucially include (and are related to) genes involved in brain rhythmicity. We will claim that this translational effort and the links we uncover may help develop an understanding of language evolution, along with the etiology of schizophrenia, its clinical/linguistic profile, and its high prevalence among modern populations.

Neurobiología y neurogenética de la dislexia

INTRODUCTION Dyslexia is a learning disability in which reading (but not any other) impairment is the most prominent symptom. There seems to be a high comorbidity among dyslexia and other learning disabilities, such as SLI, SSD or ADHD. DEVELOPMENT The nulear deficit in dyslexia appears to correspond to an impairment in phonological processing. Structural and functional studies in dyslexic readers converge to indicate the presence of malformations in the brain areas corresponding to the reading systems, but also a failure of these systems to function properly during reading. Genes linked (or associated) to dyslexia have been shown to be involved in neuronal migration and axon guidance during the formation of the cortex. In the developing cerebral neocortex of rats, local loss of function of most of these genes not only results in abnormal neuronal migration and neocortical and hippocampal malformations, but also in deficits related to auditory processing and learning. While the structural malformations resemble neuronal migration abnormalities observed in the brains of individuals with developmental dyslexia, processing/learning deficits also resemble deficits described in individuals affected by the disease. CONCLUSIONS On the whole, dyslexia seems to be on a continuum with typical reading at different biological levels (genetic, biochemical, physiological, cognitive). Furthermore, certain elements belonging to some of these levels (mainly -some of the- genes linked or associated to the disease, but also -some of the- neuronal structures whose development is regulated by these genes) would simultaneously belong to those of other cognitive abilities, which give rise to diseases of a different nature (i.e. non- dyslexic impairments) when they are impaired.

Osteogenesis and neurogenesis: a robust link also for language evolution

This paper seeks to contribute to the characterization of the relation between osteogenesis and neurogenesis by approaching it from the field of the neurobiology of language and cognition; specifically, from an evolutionary perspective. It is difficult to ascertain how the hominin brain changed to support modern language and cognitive abilities because we can only rely on skull remains. But insights can be gained from fossils because the brain and the skull exhibit a tight relationship. Skull shape and brain shape and connectivity influence one another (Roberts et al., 2010; Lieberman, 2011). Craniofacial anomalies and cognitive disorders frequently co-occur (see Boeckx and Benitez-Burraco, 2014a for review). So, “osteo” considerations can shed light on “neuro” considerations (and vice versa). Importantly, main differences between anatomically-modern humans (AMHs) and Neanderthals pertain not to the brain size, but to the more globularized headshape of the former (Bruner, 2004). Globularity results from an AMH-specific developmental trajectory after birth, at a stage when the brain is the primary determinant of skull shape (Gunz et al., 2010). Globularization is not just a morphological change of the skull. On the contrary, factors giving rise to globularity also have important neurofunctional consequences. The hypothesis we have explored in our recent work is that the rewiring of the hominin brain associated to globularization brought about our most distinctive mode of cognition (see Boeckx and Benitez-Burraco, 2014a for details).