FRIDAY, Dec. 28 (HealthDay News) -- Many of the neurological and psychiatric symptoms of Fragile X syndrome, the most common inherited cause of mental retardation, can be reversed by reducing the expression of a gene unrelated to the underlying genetic defect of the disease in mice, according to the results of a study published in the Dec. 20 issue of Neuron.
Gul Dolen, Ph.D., from the Massachusetts Institute of Technology in Cambridge, Mass., and colleagues generated mice lacking the FMR1 gene, whose silencing is responsible for Fragile X syndrome, and with a 50 percent reduction in the expression of mouse GluR5, a metabotropic glutamate receptor. They then studied various phenotypes related to human Fragile X syndrome.
The researchers found that the excessive sensitivity to environmental change, synaptic connectivity, protein synthesis, memory extinction, body growth and excitability found in mice lacking FMR1 could be corrected by reducing GluR5 expression.
"Our results demonstrate that mGluR5 contributes significantly to the pathogenesis of the disease, a finding that has significant therapeutic implications for Fragile X and related developmental disorders," Dolen and colleagues conclude.
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