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The Genetics of Language

Capabilities Text to speech. Additional information Publisher Taylor and Francis. Publisher Taylor and Francis. They have also tried to teach chimpanzees, bonobos, gorillas, and orangutans to use symbols, lexigrams, and sign language, and a few poster apes like Koko, Washoe, and Kanzi have no small measure of fame thanks to PBS documentaries, magazine cover stories, and books about their communication skills.

Some have even shown what appears to be a remarkable ability to understand spoken words. Nevertheless, an impassable border separates our speech and language abilities from theirs. The best-trained apes can learn only a few hundred words. Most any human three-year-old has a larger vocabulary, and the average high-school graduate has a mental lexicon of about 60, words.

In the hope of beginning to explain this discrepancy, Geschwind investigated which genes are turned on in the brains of humans and in those of chimpanzees, our closest genetic relatives. He found hundreds of differences but had no way to determine which ones mattered—which were most significant in driving evolution and determining brain function.

Toward a Genetics of Language

Rather than looking at differences between individual genes, they analyzed differences between networks of genes expressed at the same time. Diagrams of the networks look much like maps of airline routes, and both the human and chimp maps have a ridiculous number of hubs and spokes. But the diagrams make it easy to see the most important genes—those at the hubs. And when the team took the human map of a module and removed all the chimp connections for the same module, only a few genes were left.

It became startlingly clear not only which genes are uniquely human, but also which of those are most important. Geschwind is hopeful that taking a broader view of not only the genome but also the transcriptome—the set of genes that are turned on at any given time—will lead to more insights into the genetics of language. They found that the protein made by the FOXP2 gene in chimps is virtually identical to that made in mice: Biologists believe that if proteins undergo little alteration over an evolutionary span of tens of millions of years, they must perform such essential functions that they simply cannot tolerate change.

But two amino acids in human FOXP2 differ from those in the chimp protein—a total of three changes from the mouse version. That the gene withstood such dramatic change in such a short time span evolutionarily speaking suggests that the change helped us survive—as the development of language surely did. Although they have yet to sequence the entire gene, they found that Neanderthals and modern humans matched at the two critical spots that separate humans and chimpanzees.

Though often depicted as knuckleheads, our closest hominid relatives may have shared at least some of our capacity for speech and language. But he adds that the many unknown genes involved in language will eventually have to be found and looked at in Neanderthals. Geschwind is continuing his hunt for those unknown genes, applying to his behavioral-genetics work the technique he developed to compare human and chimp gene expression. His lab is now doing the same sort of coexpression studies on brains from healthy humans and schizophrenics, which he hopes will uncover connections that are broken in schizophrenia and perhaps lead to still more genetic pathways related to speech and language.

He hopes eventually to do similar analyses with autopsied brains from people who had autism-spectrum disorders. Still, confidence is building that in the not-too-distant future, scientists will be able to write a lengthy book about how we evolved our phenomenal gift of gab, highlighting the critical suites of genes that make it possible.

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Subscribe now for unlimited access to online articles. Why we made this change Visitors are allowed 3 free articles per month without a subscription , and private browsing prevents us from counting how many stories you've read. Rewriting Life The Genetics of Language Researchers are beginning to crack the code that gives humans our way with words.

Researchers are searching for the genes that wire these regions and produce the uniquely human capacity for speech. All things considered, new perspectives are needed regarding the mechanisms that govern growth in language acquisition for children with SLI, and the nature of the weaknesses that lead to prolonged deficits in language acquisition that persist into adolescence and beyond.

The growth curves point to three important distinctions: One is the onset of change, when a particular property of language acquisition begins to grow over time; the second is the trajectory of growth once activated; the third is an apparent deceleration or leveling of language levels that appears in early adolescence.

These properties have analogs in biological mechanisms, under gene regulation. The immune system provides an example of how onset, acceleration and deceleration can function at the cellular level.


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T cells are a type of white blood cell that destroys infected cells that are recognized as foreign. A recent discovery reveals that T cells require two signals to attack a target effectively: The sequence includes a cumulative braking function, to ensure that the immune response does not over-react to perceived threats. This is accomplished by molecules produced in the sequence that eventually inhibit T cell activity.

Recent genetic studies provide some clues. There is growing evidence of likely genetic influences on SLI. Twin studies provide strong evidence of heritability of SLI in children, based on behavioural comparison of pairs of monozygotic and dizygotic twins Dale et al. More recently, candidate gene investigations with probands and their families yield discoveries at the molecular level that draw attention to possible gene effects. Behavioural phenotypes are the measured traits that result from gene expression as well as the influence of environmental factors and the interaction between the two.

The relevant recent studies have used several kinds of phenotypes: Classification of children as SLI; performance levels on omnibus language tests or tests of vocabulary and grammar; age of first words; and reading levels. Approximately half of young children with SLI go on to develop reading impairments when they reach the age of reading instruction Catts, Given this overlap of impairments, a reading phenotype could identify candidate genes for shared genetic influence on language and reading. Several outcomes of interest are briefly summarized here.

Detailed reviews of current discoveries can be found in recent papers Paracchini, ; Smith, Relevant candidate gene association studies calculated the statistical probability that a behavioural phenotype co-occurred with a genetic variation measured at the molecular level of single nucleotide polymorphisms SNPs, defined as variations in sequences of the basic components of DNA: One gene of interest is KIAA , a candidate gene with two studies replicating associations of SNP variants located on this gene with language impairment phenotypes in different samples of children with SLI and their families Newbury et al.

Because this kind of investigation is relatively new, the demands for data collection are high, and few studies have been reported, the replication across two studies for a particular molecular location is important. Although the replication is encouraging, the outcomes are not definitive due to small sample sizes that need further replication.

This gene, KIAA, has particularly interesting properties. The gene is reported to influence neuronal migration in embryonic rat brain, suggesting possibly similar effects in humans that remain to be established. In addition, KIAA is thought to play a role in the etiology of reading disability.

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Recent investigation has identified mechanisms of gene expression of KIAA that could regulate the effects of other genes, providing support for a possible regulatory role for this gene Couto et al. Variants of this gene are significantly associated with performance of children with SLI on a non-word repetition task, which in turn is associated with performance on language assessments Vernes et al.

The chain of evidence does, however, support the plausibility of such a claim cf. A possible link between growth trajectories of language in children with and without SLI and their genes requires closer consideration of molecular levels of gene expression. In many ways the functions of genes or, more generally, DNA and RNA are intrinsically timed, in well synchronized complex chemical interactions.

Genes can be grouped into two types. This suggests the possibility that if promoters or enhancers are slow to activate a gene function that is necessary in the causal pathway, perhaps in the development of cortical structures needed for the beginnings of language acquisition, then language onset could be delayed. The example of the distinct signals in the immune system, in the functioning of T cells, indicates that such signaling systems can be differentiated for onset, acceleration, and deceleration, leading to delayed onset, spared acceleration once onset is established, but a limited time window before deceleration begins.

Thus, there are parallels between the molecular mechanisms of gene expression and the observed patterns of language growth in children with SLI and unaffected children. Another way in which timing mechanisms could enter into the causal pathways for SLI could be via epigenetic processes. Epigenetic models can be differentiated from genetic variant disease models Feinberg, Epigenetics is defined as modifications of DNA or associated proteins, other than DNA sequence variations, that carry information content during cell division. Epigenetic change is thought to be at the heart of normal development in the sense of cellular development , allowing for the likelihood that disruptions in epigenetic modifications can disturb normal developmental programs Feinberg, The model proposes an epigenetic code in the central nervous system that mediates synaptic plasticity, learning, and memory.

It is conceivable that such breakdowns could be part of the pathways to SLI, in the cascades necessary to establish the neuronal infrastructure for the onset of language acquisition, the relative sparing of subsequent acceleration, and a time-limited period of growth followed by deceleration in early adolescence. Rice hypothesizes a growth signaling dysfunction GSD , involving a breakdown in the synchronization of onset, growth, and deceleration of language acquisition and underlying neurocognitive circuits, as part of the biological basis of SLI. The causes and etiological pathways of SLI remain unknown, but progress is evident on two fronts.

Toward A Genetics of Language | Taylor & Francis Group

One front is on the behavioural level, documenting how dimensions of language change over time for children with and without SLI, revealing crucial distinctions between the start of growth, rate of change, and leveling of change over time. The same growth trajectory does not fit across different dimensions of language. Even so, the same model of growth fits children with and without SLI, once adjusted for the group differences in level of performance at the first time of measurement.

Children with SLI seem to have a delayed beginning for various dimensions of language relative to their age peers, a pattern that persists across childhood as new levels of language acquisition appear. Most striking, children with SLI, on average, increase their language levels at the same rate as children without SLI, indicating robust change over time, until they reach early adolescence when the rate of change seems to level off, leaving them with language levels below age expectations.

On another front, candidate gene studies suggest a possible role for individual variations in genes known to be involved in neuronal development. Further consideration of mechanisms and processes involved in gene expression highlight the ways in which molecular level timing functions could influence higher cognitive processes of humans, such as a decline in memory with aging.

Although there will be many challenges for the development of definitive evidence about the biological underpinnings of SLI, and ways in which environmental influences interact with these underpinnings, it is nevertheless clear that we have reason to adjust the way we think about language growth in children with SLI. Instead, children with SLI are different from and similar to children without SLI in dynamic ways, not static, involving cycles of change throughout childhood.

Even when lower levels of performance on language assessments persist over time the children are nevertheless growing in their language abilities, which clearly can grow as rapidly as in children without SLI. At the same time, an apparent braking function that depresses language growth in early adolescence would leave adolescent children with a high risk of becoming adults with SLI. The genetics evidence suggests that the children of adults with a history of SLI could inherit gene variants or variants in gene regulatory mechanisms that set up a replication of the growth trajectories from one generation to another.

Although this scenario is consistent with available evidence, multiple caveats apply: The evidence is limited by relatively small samples of participants, and limited further by relatively small samples of the complex world of possible genetic mechanisms in causal pathways. Another limitation is that means of measurement for both the behavioural growth patterns and the genetic mechanisms are relatively new, with replication studies needed.

Definitive findings await the outcomes of future investigations.

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Even at these early stages, however, there is value in a new developmental perspective on language growth for the work of speech-language pathologists. A truly developmental perspective could impact essential components of intervention, such as the identification of goals for language intervention, determination of when to intervene for particular linguistic structures, expected rates of change, interactions with family members, and presumed causal mechanisms for SLI.

Each of the components could benefit from an awareness of the need to consider a growth perspective. Special appreciation is extended to the Speech Pathology Association of Australia and the organizers of the Speech Pathology Australia national conference, held in Hobart, Australia, 24—27 June, National Center for Biotechnology Information , U. Int J Speech Lang Pathol. Author manuscript; available in PMC Jun 1.

Author information Copyright and License information Disclaimer. See other articles in PMC that cite the published article.


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  • Abstract Behavioural studies of children with specific language impairment SLI have reported long term growth outcomes across different dimensions of language. Genetics, language impairment, specific language impairment, language growth, language phenotypes, typical language development. Introduction Children with language impairments are identified on the basis of language performance levels lower than expected relative to their age peers.

    Children with Specific Language Impairment Language impairments can appear in children with or without other disabilities. Growth patterns across dimensions of language for affected and unaffected children Children with SLI identified when young are likely to persist in a low level of language performance on standardized instruments, relative to their age peers, as they move through childhood Johnson et al.

    Omnibus standard scores are not sensitive to details of growth across different dimensions of language In the program of investigation reported here, child assessments for the growth analyses were designed to yield meaningful raw scores that track progress toward the adult grammar. Open in a separate window. Questions raised by growth patterns Much of the literature has focused on accounting for the language acquisition weaknesses of children with SLI, relative to their age peers.

    Candidate gene studies of reading and language abilities There is growing evidence of likely genetic influences on SLI. Gene regulation mechanisms as future directions A possible link between growth trajectories of language in children with and without SLI and their genes requires closer consideration of molecular levels of gene expression.

    Conclusions and clinical implications The causes and etiological pathways of SLI remain unknown, but progress is evident on two fronts.


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    Peabody Picture Vocabulary Test. American Guidance Service;