Experiments in mice have raised the hope that some of the developmental delays that are part of the condition may be eradicated. When foetal mouse pups that had a syndrome similar to Down’s were treated with nerve-protecting chemicals some of the delays were removed.

Children with Down’s Syndrome have an extra copy of chromosome 21, while mice engineered to have a similar condition are given an extra copy of a segment of chromosome 16. Both result in the development of certain motor and sensory abilities being delayed, together with differing degrees of learning disability.

If the neurotransmitter GABA is inhibited in the mice, their learning ability can be improved. From this, it is believed that if children with Down’s Syndrome were treated before being born their cognitive potential could be improved.

Previous research in both mice and people with Down’s Syndrome has revealed malfunctions in the glial cells. These are brain cells that regulate the development of neurons (nerve cells) by releasing certain proteins known as NAP and SAL. This malfunction results in less of these proteins being produced than normal. When segments of these proteins are added to cultured neurons from people with Down’s Syndrome the neurons appear protected and less liable to degeneration.

This new research was carried out by Catherine Spong and her colleagues at the National Institute of Health in Bethseda, Maryland, and involved injecting the proteins NAP and SAL into mice pregnant with pups with the extra chromosome. When the pups were born, they reached developmental milestones at the same time as normal mice. A significant amount of delay was prevented.

In addition the brains of the treated mice also showed normal levels of ADNP – a regulatory protein which is underproduced by Down’s affected glial cells, and of another compound that is a marker for healthy glial cells. Both findings indicate that some effects of Down’s had been removed.

It must be remembered that what works in mice or cultured human cells doesn’t always work in people but the research is producing some cautious optimism.

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New Scientist; 26 November 2008