Toward A Genetics of Language

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. 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.

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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. 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.

American Journal of Human Genetics. An integrated epigenetics and genetic approach to common human disease. Trends in Genetics, Harvard University Press; Language impairments and reading disabilities. Developmental trajectories of verbal and nonverbal skills in individuals with a history of Specific Language Impairment: From childhood to adolescence.

Journal of Speech, Language, and Hearing Research. Genetic influence on language delay in two-year-old children. Epigenetic mechanisms in cognition. High heritability as a function of more severe cases. Peabody Picture Vocabulary Test. American Guidance Service; Genetics and phenotypic effects of phonological short-term memory and grammatical morphology in specific language impairment.

Genes, Brain, and Behavior. Epigenetics at the epicenter of modern medicine. Journal of the American Medical Association. Complexities and constraints in nonword repetititon and word learning. Apr 23, The T-cell army; pp. Linking outcomes from Peabody Picture Vocabulary Test forms using item response modeling. The SPCH1 region on human 7q Genomic characterization of the critical interval and localization of translocations associated with speech and language disorder. Children with specific language impairments. Speed of processing, working memory, and language impairment in children.

Investigation of dyslexia and SLI risk variants in reading- and language-impaired subjects. Dissection of genetic associations with language-related traits in population-based cohorts. Journal of Neurodevelopmental Disorders. A theoretical molecular network for dyslexia: A unified model of specific and general language delay: Grammatical tense as a clinical marker of unexpected variation. Levy Y, Schaeffer J, editors. Language competence across populations: Toward a definition of specific language impairment.

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Mean length of utterance levels in 6-month intervals for children 3 to 9 years with and without language impairments. Tense marking in children with autism.

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The pace of vocabulary growth helps predict later vocabulary skill. Novel cancer immunotherapy agents with survival benefit: Approach to epigenetic analysis in language disorders. Finiteness marking in boys with Fragile X Syndrome. Heritability of poor language achievement among twins. Journal of Speech, Language and Hearing Research.

The prevalence of specific language impairment in kindergarten children. Francks and his colleagues could not corroborate that suggestion, but they did find a region of chromosome 2 that seemed linked to left-handedness.

They then examined the DNA of pairs of healthy left-handed brothers: Adding still more bizarre connections, the team performed a study of siblings with schizophrenia, which implicated the same region. To find the gene or genes at the heart of this knot of links, the researchers compared the same region of chromosome 2 in healthy right-handed people, healthy left-handed people, and people with schizophrenia. They found four DNA differences that distinguished the schizophrenics from the mentally healthy lefties; the location of these variations led them to a gene called LRRTM1.

Geschwind collaborated in the work that helped identify where in the human brain LRRTM1 was turned on, or expressed: He suspects that in early gestation, it also contributes to brain asymmetry. Presumably, reduced levels of LRRTM1 could have contributed to reduced brain asymmetry, tilting the developmental scales toward left-handedness and schizophrenia—and potentially toward a variety of speech and language problems. All this adds up to little more than a list of genes that may or may not be involved in creating speech and language: To that end, Geschwind and others are turning to evolutionary studies that analyze these genes in other species and compare them with the human versions.

Such studies may also provide clues to how humans evolved the capacity for language. The Origin of Speech Like songbirds, dolphins, whales, bats, elephants, and—of course—humans, monkeys and apes can learn sounds and use them to communicate. For many decades, researchers have attempted to decode such animal messages. 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.

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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.

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. No one's rated or reviewed this product yet. Skip to main content. Toward A Genetics of Language. The past decade has brought important new advances in the fields of genetics, behavioral genetics, linguistics, language acquisition, studies of language impairment, and brain imaging.

Although these advances are each highly relevant to the determination of what a child is innately prepared to bring to language acquisition, the contributing fields of endeavor have traditionally been relatively self-contained, with little cross communication. This volume was developed with the belief that there is considerable value to be gained in the creation of a shared platform for a dialogue across the disciplines.