Washington - US researchers say they have successfully corrected key symptoms of a type of autism and mental retardation in mice, a development which could offer sufferers a potential treatment.
The tests carried out on mice aimed to correct "Fragile X syndrome," which affects about 100 000 Americans, said the study from the Massachusetts Institute of Technology (MIT) to be published on Thursday in Neuron magazine.
Fragile X syndrome is the most common inherited cause of autism and mental retardation, which can be manifested in childhood epilepsy and abnormal growth.
It is caused by the loss of a gene, known as the "fragile X mental retardation protein" (FMRP), which is believed to act as a brake on synthesizing proteins in the brain.
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The team used genetic engineering Researchers sought to prove that the loss of this protein allowed another one that stimulates protein synthesis, known as mGluR5, to act unchecked.
Genetic engineering tests proved that cutting the amount of mGluR5 in mice helped to reduce the abnormalities caused by the loss of the other key protein, such as the number of epileptic fits.
"Fragile X is a disorder of excess synaptic connectivity, protein synthesis, memory extinction, body growth, excitability - and remarkably all these excesses can be reduced by reducing mGluR5," said the study's lead author Mark Bear, from the MIT's Picower Institute for Learning and Memory.
Although the team used genetic engineering to reduce the amount of mGluR5 in the mice, the research offers a hope of treatment by using a certain class of drugs which will soon be going on trial.
"Insights gained by this study suggest novel therapeutic approaches, not only for fragile X but also for autism and mental retardation of unknown origin," added Bear.
Fragile X Syndrome is passed down on the mother's genes and affects one in 4 000 boys. Those affected can be hyperactive or have a tendency towards autism.
There are also certain facial characteristics such as an elongated face, and large, sticking-out ears.
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