Researchers have successfully corrected key symptoms of mental
retardation and autism in mice, which could be a potential
treatment for sufferers, according to a study in Neuron
magazine on Thursday.
Researchers from the Picower Institute for Learning and Memory
at the Massachusetts Institute of Technology (MIT) carried out the
tests on mice aimed to correct "Fragile X syndrome," which affects
some 100,000 Americans.
"These findings have major therapeutic implications for Fragile
X syndrome and autism," said lead author Mark Bear, director of the
Institute.
Fragile X syndrome is the most common inherited cause of autism
and mental retardation, which can be passed down on the mother's
genes and affects one in 4,000 boys.
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.
Researchers sought to prove that the loss of this protein
allowed mGluR5 to act unchecked, which stimulates protein
synthesis.
The 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 Bear.
The work indicated that a certain class of drugs could have the
same effect with interference with mGluR5, the researcher
noted.
But, these drugs are not yet approved, which are expected to go
into human safety trials in America next year.
(Agencies via Xinhua December 20, 2007)