FOXP2 AND THE NEUROANATOMY OF SPEECH AND LANGUAGE PDF

Faurg Log In Sign Up. Accelerated protein key players in development and metabolism. Detecting bilateral abnormalities with Moreover, the overall speecu statistical criteria than the ones adopted in these pattern of FoxP2 expression in the brain of the zebra finch24 is remarkably similar to the studies might have led to the inclusion of other areas of pattern in mammalian brains, including the brain of the human fetus see text. The more strongly express the gene — notably a subset of lateral rostral of the two pathways that make up this circuit forms a loop homologous to the languagr and lateral temporoparietal cortical areas, and frontal—basal ganglia loop langkage in FIG. By considered to provide initial hypotheses. The expression and articulation of language more than its new chapter began with an investigation of three gener- comprehension, and problems were noted with neuronaatomy ations of the KE family, half of whose members have a nizing and coordinating the high-speed movements VERBAL DYSPRAXIA that is inherited in a pattern consistent that are necessary for the production of intelligible with an autosomal dominant mutation.

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Metrics details Key Points Familial disorders of speech and language provided early evidence that genetic mutations could impair these abilities, but a causative mutation in a single gene was only recently identified. Mutations in FOXP2 cause an inherited verbal dyspraxia associated with an orofacial movement disorder in a family known by the label KE.

Although the behavioural phenotype has been carefully studied, it is still unclear whether all the effects of the mutation are caused by a single core deficit in orofacial movement, or whether there are additional core deficits that can account for the grammatical, semantic and cognitive impairments that are found in affected family members.

Functional neuroimaging studies have also shown some abnormalities in patterns of activation. FOXP2 encodes a transcription factor that is expressed in the brain, lungs, heart and gut.

In the brain, it is widely expressed in sensory, limbic and motor structures. We assume that the circuitry that underlies normal speech is similar to the frontostriatal and frontocerebellar circuits that modulate and control the motor cortex in the performance of other types of movement. Most of the areas in the proposed circuit express FOXP2, and several of these show abnormalities in affected members of the KE family. Much work is needed to clarify the details of the deficits caused by mutations in FOXP2 and to provide evidence that supports or contradicts our proposed circuitry.

This work will involve behavioural, imaging, gene expression and gene knockout studies. Abstract That speech and language are innate capacities of the human brain has long been widely accepted, but only recently has an entry point into the genetic basis of these remarkable faculties been found. The discovery of a mutation in FOXP2 in a family with a speech and language disorder has enabled neuroscientists to trace the neural expression of this gene during embryological development, track the effects of this gene mutation on brain structure and function, and so begin to decipher that part of our neural inheritance that culminates in articulate speech.

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FOXP2 AND THE NEUROANATOMY OF SPEECH AND LANGUAGE PDF

Metrics details Key Points Familial disorders of speech and language provided early evidence that genetic mutations could impair these abilities, but a causative mutation in a single gene was only recently identified. Mutations in FOXP2 cause an inherited verbal dyspraxia associated with an orofacial movement disorder in a family known by the label KE. Although the behavioural phenotype has been carefully studied, it is still unclear whether all the effects of the mutation are caused by a single core deficit in orofacial movement, or whether there are additional core deficits that can account for the grammatical, semantic and cognitive impairments that are found in affected family members. Functional neuroimaging studies have also shown some abnormalities in patterns of activation. FOXP2 encodes a transcription factor that is expressed in the brain, lungs, heart and gut.

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FOXP2 and the neuroanatomy of speech and language.

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