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May 24, 2007
Putting the Hex on Fragile X
A stimulating environment
can undo the physiological effects of mental retardation in
laboratory mice, researchers have found. The discovery might pave
the way toward similar therapy for children afflicted with
a similar kind of retardation called Fragile X syndrome,
although the parallels with the human condition aren't perfect.
Fragile
X is one of the most common causes of
mental retardation, generated by the inheritance of a defective
gene called fmr1. Affecting about one in 4000 people,
its manifestations include diminished abilities to learn and memorize,
as well as anxiety in the presence of strangers
and an overall stressful disposition. In the new experiments,
researchers from VU University in Amsterdam, the Netherlands, used
lab mice containing the deactivated fmr1 gene. These mice
also have learning deficiencies.
First, the scientists set out to
identify the underlying neurological defect in the mice. To
do so, they analyzed mouse nerve cells from the
prefrontal cortex--an important part of the brain for learning
and memory. These cells showed a diminished capacity to
store information for more than a few minutes, a
trait known in normal individuals as long-term potentiation. They
found that the defect lengthens a part of neurons
called the dendritic spine, which makes it more difficult
for the cells to transfer calcium ions, a critical
ability for maintaining strong electrochemical signals between neurons.
After 2
months, they detected long-term potentiation in the prefrontal cortex
cells. In other words, although Fragile X syndrome tends
to inhibit brain cells from storing information, the research
shows that exposing Fragile X mice to stimulating environments
improves the communication between the nerve cells, says neuroscientist
and co-author Huib Mansvelder. He says the new findings,
reported in today's issue of the journal Neuron, "provide
strong scientific support" to investigate in Fragile X patients
"what the best way would be to challenge these
patients and stimulate brain activity." He adds that the
approach might even benefit victims of other forms of
learning deficiencies as well.
Cell biologist William Greenough of the
University of Illinois in Urbana-Champaign remains somewhat skeptical. Although
he thinks the study provides a "plausible mechanism" for
overcoming the effects of Fragile X syndrome in mice,
"when it comes to enriching the environment in a
human home, I think many parents have tried to
provide stimulation and the effects have been much less
dramatic," he says.
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