FOXP2 AND THE NEUROANATOMY OF SPEECH AND LANGUAGE PDF

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Uusi haku. A-Z tietokannat. Kirjaston kokoelmat. Painetut julkaisut. Tarkennettu haku. Katso kaikki. Gadian ; Andrew Copp ; Mortimer Mishkin ;.

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Tarkat tiedot. FOXP2 and the neuroanatomy of speech and language. Faraneh Vargha-Khadem. David G. Andrew Copp. Mortimer Mishkin. Nature Reviews Neuroscience, , Vol. Foxp2 Protein. Motor Systems. Magnetic Resonance Imaging. Cognitive Ability. Transcription Factors. Movement Disorders. Structure-Function Relationships. Broca'S Area. Precentral Gyrus. Neurobiology of Language. 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.

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. MRI scans of affected individuals showed no obvious focal abnormalities on conventional neuroradiological assesments, but more detailed analyses have revealed reductions in the volumes of several brain areas that are involved in motor functions, including the caudate nuclei, Broca's area, the precentral gyrus and the ventral cerebellum.

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.

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FOXP2 and the neuroanatomy of speech and language

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FOXP2 and the Neuroanatomy of Speech and Language

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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. This site needs JavaScript to work properly. Please enable it to take advantage of the complete set of features! Clipboard, Search History, and several other advanced features are temporarily unavailable. Search: Search.

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Cecilia S. Lai, Dianne Gerrelli, Anthony P. Monaco, Simon E. Fisher, Andrew J. Investigation of the neural basis of this disorder has been limited previously to neuroimaging of affected children and adults. The discovery of the gene responsible, FOXP2 , offers a unique opportunity to explore the relevant neural mechanisms from a molecular perspective.

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