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FOXP2 and the mirror system

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Abstract

An inherited deficit in spoken language has been associated with a mutation in the forkhead box P2 (FOXP2) gene on chromosome 7. A recent functional magnetic resonance imaging study has linked the deficit to underactivity in Broca's area during word generation, which in turn suggests a possible link between FOXP2 and the mirror-neuron system observed in the primate homologue of Broca's area. This link might have implications for the evolution of Broca's area and its role in speech.

Section snippets

Insights from the KE family

Evidence on the role of FOXP2 comes primarily from investigation of the deficit suffered by affected members of the KE family. One perspective has been that the deficit is primarily linguistic, particularly affecting the acquisition of morphosyntactic rules [6] – indeed, it was even hinted that FOXP2 might be the ‘grammar gene’ implied by Chomsky's theorizing [7]. Another perspective was that the deficit is primarily one of articulation and nonverbal praxis [8]. One recent study showed that the

The laterality gene?

Both the functional and morphological abnormalities caused by FOXP2 mutation appear to be bilateral. If the mutation was to affect language areas in the left hemisphere only, then one would expect affected members of the KE family to develop compensatory language networks in the right hemisphere, but this does not appear to be the case. A possible implication is that FOXP2, in its normal form, is responsible for the lateralized role of Broca's area in speech. This makes it tempting to identify

The role of Broca's area

In the discussion of their results, Liégeois et al. focus more specifically on the role of Broca's area. This area is thought to be the human homologue of area F5 in the monkey, where mirror neurons have been identified. Mirror neurons are so-named because they discharge not only when the animals make grasping movements with their hands, but also when they observe others making the same movements [14]. Moreover, it has been proposed that these neurons, now understood to be part of a more

Future perspectives

A next step in research on the KE family might be to determine whether the deficit in affected members of the KE family extends to the mirror system as a whole, or whether it is restricted to speech and/or orofacial movements. For example, one might ask whether the affected members have a deficit in copying hand movements, or if viewing hand movements activates brain circuits known to be part of the mirror system [15].

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