Abstract

Parkin and PINK1 have been well studied for their dopaminergic dysfunction in the striatum, the area most affected in Parkinson disease (PD).1,2 By definition, individuals with recessive inheritance are carriers of a single mutant allele and provide a useful model to study the impact of striatal dopaminergic cell loss on the motor systems of the human brain.1,3 Functional neuroimaging has facilitated investigation of this correlation. A recent fMRI study4 showed that mutation carriers had a stronger activation of certain cortical areas such as the right rostral cingulate and left dorsal premotor cortices with internally cued movements, providing evidence for motor reorganization in nonmanifesting carriers of the Parkin gene. In this issue of Neurology ®,1 the same investigators modified their study to engage the participants in predefined finger sequential movements to be more specific in motor reorganization and hypothesized that the dopaminergic dysfunction of these mutant carriers would cause a region-specific cortical reorganization. In addition, they included nonmanifesting individuals who were carriers …

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