A common flying insect may have opened a door for the treatment of one of the most common inherited forms of mental retardation.
In fact, the findings by University of Utah biologists may make it possible to use drugs already on the market.
The story from Science Specialist Ed Yeates.
University of Utah biologists duplicated a version of the genetic human Fragile X Syndrome in fruit flies. The condition in humans disrupts communication links in the nervous system, producing one of the most common inherited forms of mental retardation.
But when the Utah team corrected one of only two genes, the excessive growth of a hollow-like protein fiber called microtubules - which causes the defects - ended.
Kendal Broadie / University of Utah Biologist: "IF YOU CORRECT FOR THE INCORRECT REGULATION OF JUST ONE TARGET GENE - THAT RESCUES ALL OF THOSE DEFECTS. NOW THE FLIES CAN UNDERGO COMPLEX BEHAVIORS PERFECTLY NORMALLY. THE STRUCTURE OF THE NERVOUS SYSTEM IS PERFECTLY NORMAL AND THE FLOW OF COMMUNICATION WITHIN THE NERVOUS SYSTEM IS PERFECTLY NORMAL AS WELL."
ED YEATES, SCIENCE SPECIALIST: "HERE IN ALPINE, UTAH, RANDY AND TERI BECK KNOW ALL ABOUT FRAGILE X SYNDROME. ALL THREE OF THEIR CHILDREN HAVE IT. THE MOST SEVERE - THEIR YOUNGEST, KANU."
10-year-old Kanu does not talk. Autism complicates his condition even more.
His two older brothers, 13-year-old Justin and 15-year-old Mitchell also have Fragile X Syndrome. But their mental disabilities are classified as moderate.
While Teri and Randy realize the University of Utah findings are only a beginning at this point, they imagine the possibilities.
TERI BECK: "I WOULD LOVE TO BE ABLE TO KNOW WHAT MY TEN YEAR OLD BOY SOUNDS LIKE. I WOULD LOVE FOR HIM TO TALK."
RANDY BECK: "WE WOULD LOVE FOR SOMETHING TO HAPPEN FOR THEM TO BE ABLE TO LIVE A MORE TYPICAL LIFE."
The findings in the fruit flies appear to overturn an earlier theory that Fragile X Syndrome is complicated and too difficult to treat. In fact, the discovery suggests a cancer drug currently in use might eliminate the excessive growth of the microtubules and reverse the symptoms of the disorder.
The University of Utah collaborated on the study with the University of California at Berkeley.
Nov. 29, 2001
