Scientists have made a breakthrough in the study of Down's syndrome after discovering a method to prevent the chromosomal disorder in the womb itself.
In the study on mice, the scientists observed that when foetal mouse pups that had a syndrome similar to Down's were treated with nerve-protecting chemicals, some of the developmental delays that are part of the condition were removed.
AdvertisementKids with Down's 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.
In both species, the development of certain motor and sensory abilities is delayed. These "trisomic" individuals may also have learning difficulties and symptoms of Alzheimer's later in life.
The scientists found that inhibition of neurotransmitter GABA in trisomic mice can improve cognition and this could eventually be used in children.
In fact, many researchers have claimed that treating Down's before a child is born would improve cognitive potential too.
Earlier studies both of people with Down's and trisomic mice revealed malfunctions in glial cells - brain cells that regulate the development of neurons by releasing certain proteins. The aberrant cells produce less of these proteins than normal. And adding segments of some of these proteins - known as NAP and SAL - to cultured neurons from people with Down's, which would otherwise degenerate, seems to protect the neurons.
Using the above information, researchers led by Catherine Spong at the National Institutes of Health in Bethesda, Maryland, injected NAP and SAL into mice pregnant with trisomic pups in the middle of their pregnancy.
After birth, the pups reached developmental milestones such as grasping a rod, righting themselves and responding to tactile stimulation at the same time as normal mice.
"We were able to prevent a significant amount of the delay," New Scientist quoted Spong as saying.
When the pups were born, they reached developmental milestones at the same time as normal mice
The brains of the treated mice also showed normal levels of ADNP - one of the regulatory proteins 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.
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