By IANS,
Toronto : There could soon be a cure for dumbness. In a major breakthrough for treating learning and memory defects in children as well as adults, Canadian researchers have discovered a protein which plays a critical role in restoring intellectual functions of the brain.
Roderick McInnes of Toronto University and Michael Salter of the Sick Kids hospital here have discovered that the protein called Neto1 can restore memory and learning defects.
During their experiments on mice, the two researchers discovered that Neto1 is a key component of synapses – the highly specialised sites of communication between the brain’s neurons (nervous system cells).
When the researchers genetically engineered the mice to be deficient in Neto1, they found that it showed a marked decrease in learning and in the way synapses adapt to brain activity.
But when they gave the Neto1-lacking mice a drug that is being clinically tested on people with Alzheimer’s disease, they found that the mice’s learning and memory defects were restored to normal by this drug.
“We have a new player in the game. Neto1 was never considered to be involved in how nerve cells communicate with one another. Now we found out that not only is it involved … it’s critical,” a statement quoted Salter as saying.
“It’s part of a paradigm shift in neuroscience,” said co-researcher McInnes.
“Neurologists and neuroscientists have always tended to think that if the brain is abnormal at birth, nothing can be done to improve intellectual function and that special education was virtually the only assistance available.
“Our findings and other research over the past five years suggest that the situation is more hopeful. It is no longer a fantasy to think that drug treatment might, in the future, be available for such patients,” added McInnes.
Though their findings are very promising, he said it was still very early before patients with intellectual disabilities could be offered a medication.
“We would be concerned about possible negative effects, including disordered thinking or emotional disturbances, which can’t be fully evaluated in an animal model,” said McInnes.
The findings were published in the current issue of PLoS Biology.