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Rare eye-movement disorder may shed light on brain and cardiovascular development

with HOXA1 mutations were never reported in mice," says Tischfield, the study's first author. "We've potentially uncovered a new developmental role for HOXA1 in vascular patterning in humans, a role that may have been overlooked in mice."

Most intriguingly, the association of both mental retardation and autism with HOXA1 mutations suggests that early malformation of the brainstem, which controls "lower" functions such as eye movement and breathing, may also lead to impairment in higher cognitive and behavioral function.

"HOXA1 is expressed in the brainstem, but we do not believe it is expressed in the higher brain (the cerebrum or cerebellum)," Tischfield notes. "But there's a lot of output from the brainstem during brain development. Serotonin comes from the brainstem, and many people believe that autism and mental retardation result from an abnormal influence of serotonin. Our paper may spark ongoing interest in how serotonin systems modulate development of the higher brain."

Interestingly, in utero exposure to thalidomide very early in pregnancy, during the time when HOXA1 is turned on, causes damage in the brainstem that mimics the HOXA1 syndrome. In addition, a previous autopsy of an autistic individual showed brainstem pathology similar to that of mice whose HOXA1 genes had been deleted.

"HOXA1 is a gene that's been looking for a disorder for a long time," says Engle. "It's one of a series of interesting genes we've stumbled on by using complex eye-movement disorders as a marker for developmental defects."


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Contact: Aaron Patnode
aaron.patnode@childrens.harvard.edu
617-355-6420
Children's Hospital Boston
11-Sep-2005


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