The dream of treating learning disabilities with a drug is a little closer to reality now that Canadian scientists have identified a brain protein crucial to learning.

A Toronto research team discovered that this single protein, known as Neto1, helps brain cells talk to one another. If the protein is missing or not working properly, it can result in learning disabilities.

"We've identified a new molecular player that was previously completely unsuspected in being involved in how the brain works," Dr. Michael Salter, head of the neuroscience and mental health program at Sick Kids, told CTV News.

What's more, further research has found that a drug being tested in Alzheimer's patients may also help those missing this key brain cell protein.

The research is still preliminary and was cconducted on mice, so it's not clear whether the findings will translate into humans. But if they do, the discovery opens the door to the possibility that drug treatment could help those with learning disabilities.

Lead investigator, Dr. Roderick McInnes, a geneticist at the Hospital for Sick Children, made the breakthrough while hunting for genes involved in eye development in 2000. That's when he and his postdoctoral fellow David Ng came across Neto1.

"It's an unexpected surprise," McInnes told CTV Newsnet on Tuesday.

"One would hope ... similar effects might be possible some day in patients with learning disabilities," McInnes added.

Research from his lab proved the protein to be very active in sending messages between cells in the hippocampus, the part of the brain region heavily involved in memory and learning.

To find out how important the protein was to learning, the researchers decided to breed mice that were missing the gene that makes the Neto1 protein and then evaluate the cognitive abilities of those mice.

They found that the altered mice had no obvious physical or behavioural problems but did have trouble learning new skills compared to normal mice.

The mice missing Neto1 failed a simple test in which they were made to swim through a water maze and find a hidden safety platform that would get them out of the water. Normal mice swimming through the maze were able to find the platform faster with each try, but the mice missing Neto1 got lost every time and did not seem to remember how to find the platform.

Salter found the altered mice could only generate electrical signals between brain cells at half the strength of normal mice.

The researchers conclude that mice missing Neto1 have fewer receptors on their brain cells that are crucial for forming memories and learning, known as NMDA receptors.

Dr. John Roder at the Samuel Lunenfeld Research Institute at Mount Sinai Hospital then wondered if a medication now being tested in Alzheimer's patients might fix the problem.

The drugs, known as ampakines, don't increase the number of NMDA receptors, but they do seem to help them function better. In the Neto1-deficient mice, their brain cell connections were strengthened so well that they could then perform cognitive tests as well as normal mice.

Salter said the effects of the drugs were almost immediate.

But the use of ampakines for learning disabilities is still a long way off. The drugs have passed Phase 1 safety trials and are now being tested in larger Phase 2 trials to test their effectiveness for Alzheimer's patients. But it's not known when, or if, they can be tested in people with learning disabilities.

The research is published in the current issue of PLoS Biology.