scholarly journals Bridging the gap between genes and language deficits in schizophrenia: an oscillopathic approach

2016 ◽  
Author(s):  
Elliot Murphy ◽  
Antonio Benitez-Burraco
Keyword(s):  
Candidate Genes ◽  
Language Processing ◽  
Language Evolution ◽  
Gene Mutations ◽  
Human Language ◽  
Language Deficits ◽  
Modern Language ◽  
Risk Alleles ◽  
High Prevalence ◽  
Neural Dysfunction

Schizophrenia is characterised by marked language deficits, but it is not clear how these deficits arise from gene mutations linked to or associated with 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 it represents an abnormal ontogenetic itinerary for the human faculty of language, heavily rooted in the evolutionary processes that brought about modern language. To that end we will focus on how the schizophrenia brain processes language and, particularly, on its distinctive oscillatory profile during language processing: We will argue that brain rhythms constitute the best route to interpret language deficits in this condition and map them to neural dysfunction and risk alleles of the genes. Additionally, we will show that candidate genes for schizophrenia are overrepresented among the set of genes that are believed are important for the evolution of human 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 aetiology of schizophrenia, its clinical/linguistic profile, and its high prevalence among modern populations.

scholarly journals Language deficits in schizophrenia and autism as related oscillatory connectomopathies: an evolutionary account

2016 ◽  
Author(s):  
Elliot Murphy ◽  
Antonio Benitez-Burraco
Keyword(s):  
Language Evolution ◽  
Gene Mutations ◽  
Autism Spectrum ◽  
Language Deficits ◽  
Linguistic Feature ◽  
Evolutionary Account ◽  
Risk Alleles ◽  
Gene Sets ◽  
High Prevalence ◽  
The Brain

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 computes language 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.

In Search of a Human Language Processing System

1985 ◽  
Vol 30 (7) ◽  
pp. 529-531
Author(s):  
Patrick Carroll
Keyword(s):  
Language Processing ◽  
Processing System ◽  
Human Language

Clash of signs: Putting bilingualism back into language evolution

2020 ◽  
Author(s):  
Steven Samuel
Keyword(s):  
Language Evolution ◽  
Modern Human ◽  
Alarm Calls ◽  
Bilingual Children ◽  
Human Language ◽  
Typically Developing ◽  
Typically Developing Children ◽  
Modern Humans ◽  
The Real ◽  
Multiple Languages

Research and thinking into the cognitive aspects of language evolution has usually attempted to account for how the capacity for learning even one modern human language developed. Bilingualism has perhaps been thought of as something to think about only once the ‘real’ puzzle of monolingualism is solved, but this would assume in turn (and without evidence) that bilingualism evolved after monolingualism. All typically-developing children (and adults) are capable of learning multiple languages, and the majority of modern humans are at least bilingual. In this paper I ask whether by skipping bilingualism out of language evolution we have missed a trick. I propose that exposure to synonymous signs, such as food and alarm calls, are a necessary precondition for the abstracting away of sound from referent. In support of this possibility is evidence that modern day bilingual children are better at breaking this ‘word magic’ spell. More generally, language evolution should be viewed through the lens of bilingualism, as this is the end state we are attempting to explain.

scholarly journals AB0006 GENETIC RISK PROFILE FOR PSORIATIC ARTHRITIS PREDISPOSITION IN ITALIAN PATIENTS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1038.1-1038
Author(s):  
M. S. Chimenti ◽  
C. Ciccacci ◽  
G. De Benedittis ◽  
A. Latini ◽  
P. Conigliaro ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Psoriatic Arthritis ◽  
Candidate Genes ◽  
Genetic Risk ◽  
Protective Role ◽  
Risk Profile ◽  
Joint Disease ◽  
Taqman Assay ◽  
Allelic Discrimination ◽  
Risk Alleles

Background:Psoriatic arthritis (PsA) is a chronic inflammatory joint disease typically associated with psoriasis and classified in the group of spondyloarthritis (1). The pathogenesis is based on an interplay of different genes interacting with several environmental factors including stress, trauma, infections, triggering an inflammatory response related to the activation of innate and acquired immunity in different tissues and organs (2). However, the risk for the development of PsA is not clearly understood.Objectives:The aim of this study was to evaluate, in a cohort of Italian PsA out-patients of the Rheumatology Unit of the University of Rome Tor Vergata, the association of genetic variants in candidate genes for PSA susceptibility and their possible contribute in the modulation of clinical and laboratory features.Methods:The genes were selected according to previous studies describing these genes as involved in susceptibility to rheumatoid arthritis (RA) (3), since a common genetic background can be shared between these diseases. Nine SNPs (single nucleotide polymorphism) in eight candidate genes were analysed: STAT4 (rs7574865), TRAF3IP2 (rs33980500), TNFAIP3 (rs6920220 and rs2230926), MIR146A (rs2910164), PSORS1C1 (rs2233945), IL-10 (rs1800872), HCP5 (rs3099844) and ERAP1 (rs27524). Polymorphisms were analysed in 163 consecutive PsA out-patients and 198 healthy controls (HC). Genotyping was performed by allelic discrimination by TaqMan assay. Alleles frequencies differences between cases and controls or between phenotypic groups were compared using Pearson’s χ 2 test.Results:We have observed an association between PSA susceptibility and the variant alleles of STAT4 [OR= 1.60 (1.15-2.21), P= 0.005], TRAF3IP2 [OR= 1.65 (1.01-2.65), P= 0.04], ERAP1 [OR= 1.40 (1.05-1.85), P= 0.02] and TNFAIP3 (rs6920220) [OR= 1.75 (1.19-2.57), P= 0.004]. On the contrary, the variant allele of IL-10 polymorphism seems to play a protective role [OR= 0.74 (1.05-1.85), P= 0.05]. Moreover, in order to define a genetic risk profile, we have counted the total number of risk alleles in each subject, considering as risk alleles the allelic variant of rs7574865 (STAT4), rs33980500 (TRAF3IP2), rs6920220 (TNFAIP3) and rs27524 (ERAP1) SNPs. Then, we have compared the risk allele number distribution between patients and HC (Fig.1). Classes with 3 or more risk alleles are significantly more represented in patients than in HC (OR= 2.03, P=0.004). The risk to develop the disease increases significantly in subjects with at least four risk alleles (OR= 2.96, P=0.002).Figure 1.Number of risk alleles in patients and controls: rs7574865 (STAT4), rs33980500 (TRAF3IP2), rs6920220 (TNFAIP3) and rs27524 (ERAP1) SNPs.Conclusion:We confirm the associations between five SNPs, already studied in RA, and PSA susceptibility, suggesting a common inflammatory pathway in chronic inflammatory rheumatological diseases. Moreover, we show how the genotyping of only few associated SNPs could help to define a genetic risk profile for PSA development.References:[1]Calabresi E, et al. One year in review 2019: psoriatic arthritis. Clin Exp Rheumatol. 2020;38:1046-55.[2]Chimenti MS, Triggianese P, De Martino E, Conigliaro P, Fonti GL, Sunzini F, Caso F, Perricone C, Costa L, Perricone R. An update on pathogenesis of psoriatic arthritis and potential therapeutic targets. Expert Rev Clin Immunol. 2019 Aug;15(8):823-836.[3]Ciccacci C, et al. Polymorphisms in STAT-4, IL-10, PSORS1C1, PTPN2 and MIR146A genes are associated differently with prognostic factors in Italian patients affected by rheumatoid arthritis. Clin Exp Immunol. 2016;186:157-63.Disclosure of Interests:None declared

scholarly journals The integration hypothesis of human language evolution and the nature of contemporary languages

2014 ◽  
Vol 5 ◽  
Author(s):  
Shigeru Miyagawa ◽  
Shiro Ojima ◽  
Robert C. Berwick ◽  
Kazuo Okanoya
Keyword(s):  
Language Evolution ◽  
Human Language

scholarly journals Low Prevalence of Pneumocystis pneumonia (PCP) but High Prevalence of Pneumocystis dihydropteroate synthase (dhps) Gene Mutations in HIV-Infected Persons in Uganda

PLoS ONE ◽  
2012 ◽  
Vol 7 (11) ◽  
pp. e49991 ◽  
Author(s):  
Steve M. Taylor ◽  
Steven R. Meshnick ◽  
William Worodria ◽  
Alfred Andama ◽  
Adithya Cattamanchi ◽  
...  
Keyword(s):  
Gene Mutations ◽  
Pneumocystis Pneumonia ◽  
Dihydropteroate Synthase ◽  
High Prevalence ◽  
Dhps Gene ◽  
Low Prevalence

scholarly journals Human language evolution: a view from theoretical linguistics on how syntax and the lexicon first came into being

Primates ◽  
2021 ◽  
Author(s):  
Haruka Fujita ◽  
Koji Fujita
Keyword(s):  
Language Evolution ◽  
Animal Cognition ◽  
Action Planning ◽  
Theoretical Background ◽  
Human Language ◽  
Motor Action ◽  
Cognitive Capacities ◽  
Gradual Evolution ◽  
Recent Developments ◽  
Evolutionary Continuity

AbstractHuman language is a multi-componential function comprising several sub-functions each of which may have evolved in other species independently of language. Among them, two sub-functions, or modules, have been claimed to be truly unique to the humans, namely hierarchical syntax (known as “Merge” in linguistics) and the “lexicon.” This kind of species-specificity stands as a hindrance to our natural understanding of human language evolution. Here we challenge this issue and advance our hypotheses on how human syntax and lexicon may have evolved from pre-existing cognitive capacities in our ancestors and other species including but not limited to nonhuman primates. Specifically, we argue that Merge evolved from motor action planning, and that the human lexicon with the distinction between lexical and functional categories evolved from its predecessors found in animal cognition through a process we call “disintegration.” We build our arguments on recent developments in generative grammar but crucially depart from some of its core ideas by borrowing insights from other relevant disciplines. Most importantly, we maintain that every sub-function of human language keeps evolutionary continuity with other species’ cognitive capacities and reject a saltational emergence of language in favor of its gradual evolution. By doing so, we aim to offer a firm theoretical background on which a promising scenario of language evolution can be constructed.

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