As humans typically inherit 46 chromosomes, half from each parent, the fetuses afflicted by the Down’s syndrome carry an extra copy of Chromosome 21 instead of the usual two.
The syndrome is typically associated with impaired cognitive ability and physical growth. Characteristic symptoms include mild to moderate mental retardation and unusual facial appearance. Afflicted also stand a high risk of heart defects.
In the rodent study, mice were genetically engineered to have a similar condition as that of Down’s syndrome in humans. They were given an extra copy of chromosome 16.
An extra copy of chromosome 16 triggers similar motor and sensory delays in mice as an extra copy of chromosome 21 does in humans.
Immediately upon hitting pregnancy’s midterm, the pregnant mice whose fetal pups showed signs of Down’s were then injected with nerve-protecting proteins – the NAP and SAL. In Down’s, the aberrant nerve cells are known to produce less of these proteins.
After birth, the mice pups showed no signs of Down’s. More importantly, they reached their "developmental milestones" such as grasping a rod, responding to tactile stimulation and righting themselves at the same time as normal mice.
Also, the production of ADNP protein which is typically under-produced in Down’s was now being produced at normal levels, researchers highlighted.
"We were able to prevent a significant amount of the delay" lead researcher, Catherine Spong, wrote in the journal Obstetrics and Gynaecology.
The researchers are now following the mice further into childhood to see if the treatment’s effects are long-lasting. However, it is too soon to draw implications of the study in the human environment, researchers noted.
Named after John Langdon Down, a British doctor who described the syndrome in 1866, Down’s syndrome is a chromosomal disorder affecting one of every 733 babies born in the United States.
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