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Drug offers hope for Down’s syndrome
by Jamie Anderson - November 19, 2009 - comments
A drug trial conducted in a mouse model of the disease promises to thwart the complications of Down’s syndrome, a chromosomal disorder that impairs cognitive development in humans
Los Angeles, CA, November 19 -- In a remarkable medical breakthrough, a team of researchers from the Stanford University, Calif., claim to have developed a drug which increases the levels of norepinephrine, a message-carrying chemical in the brain, thus easing the learning difficulties caused by Down’s syndrome, a chromosomal disorder which affects 5,000 newborns in the United States each year.
The drug currently tested on rodents helped prevent some of the deficits of the memory in Down syndrome, displaying improvement in their thinking ability, researchers claimed.
Hoping to mimic similar results in children, study’s head, Dr Ahmad Salehi of the Veterans Affairs Palo Alto Health Care System said, "If you intervene early enough, you will be able to help kids with Down syndrome to collect and modulate information."
"Theoretically, that could lead to an improvement in cognitive functions in these kids" Salehi emphasized.
The results of the study feature in the Nov. 18 issue of the journal Science Translational Medicine.
About Down’s syndrome
Down’s syndrome is a chromosomal disorder caused by the presence of an extra 21st chromosome commonly picked-up with amniocentesis during pregnancy or at time of birth.
Down’s syndrome is typically associated with impaired cognitive ability and physical growth. However, other health concerns include a pronounced risk for congenital heart defects, gastroesophageal reflux disease, frequent ear infections, obstructive sleep apnea, and thyroid dysfunction.
The study
Genetically mutated mice, those that had an extra copy of chromosome 16 were picked up for the study. An extra, third copy of 104 genes on chromosome 16 is homologus to genes on human chromosome 21, dispelling similar mental disabilities researchers explained.
Like humans, mice with Down-syndrome-like-dysfunction had deficit levels of norepinephrine in the brain, the problem primarily occurring in the part of the brain called the locus coeruleus responsible for producing and supplying norepinephrine to other parts of the brain, the neurotransmitter essential for learning and memory function.
The deficiency inhibited mice to exhibit normal behaviors i.e. when placed in a strange cage they failed to build nests, something what normal mice did.
The mice were then administered a dose of the new drug that boosted the levels of norepinephrine in the brain. Surprisingly, within a few hours of getting the requisite dose the mice created nests, an act on par with those of normal mice.
But unfortunately the positive effects did not last that long. Once the effects waned, the mice bounced back to typical Down’s behavior, researchers highlighted.
"The findings give a ray of hope and optimism for the Down syndrome community for the future" Dr Melanie Manning, director of the Centre for Down’s syndrome at Lucile Packard Children's Hospital, in San Francisco said.
"It's very exciting. We still have a long way to go, but these are very interesting results" Manning marked.