Possible Treatment for
Down's Syndrome Retardation may Involve Interference with Gene - Same
Gene might Cause Alzheimer's
July 6th 2006
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Stanford
University researchers believe they may be able to “reverse the
cognitive decline” that frequently affects those with Down’s syndrome in
middle age. "We may now have the opportunity to make a big difference
in people's lives," according to neurologist William Mobley, MD, PhD.
"If we can decrease the expression of this gene we may be able to
provide something more than supportive care to people with Down
syndrome."
Mobley and his
team believe they have found the gene that when overexpressed, causes
neurons responsible for attention and memory to shrivel and stop
functioning normally. It may be possible to “interfere” with the gene.
Down’s syndrome is
the leading cause of mental retardation in the United States. There are
more than 300,000 people nationwide have Down syndrome, which is caused
by an extra copy of chromosome 21, giving them a total of three. Up
until now, there has been little molecular or Neurological research done
on the subject.
There are many
symptoms associated with the disorder. "Down syndrome results in an
extraordinarily complex constellation of symptoms," said lead author and
senior research scientist Ahmad Salehi, MD, PhD. "We've done what many
people thought was impossible: We've dissected it genetically to
correlate one of the most troubling symptoms - cognitive dysfunction -
with one particular gene. While it's not the only gene involved, its
presence in three copies makes a significant difference."
The same gene that
has been identified with the early-onset Alzheimer's disease, called App
for amyloid precursor protein, is directly linked to degeneration of a
specific group of neurons in the brains of those with Down syndrome.
This research confirms earlier research. Neuronal degradation in people
with Down syndrome is the result of an interrupted conversation between
nerve cells in a specific part of the brain.
The researchers
compare the problem with the classroom troublemaker. They say the
signaling neuron needs feedback to thrive. The neuron lobs specialized
compounds called neurotransmitters toward its neighbor and awaits a
response to its molecular “spit wads”. The target cells then fire back
a set of molecules, or nerve growth factor (NGF). The NGF is engulfed
by the membrane of the instigator cell and is shuttled to the cell body
in a process called retrograde transport. Once there it acts on the
nucleus to stimulate the expression of genes that support neuronal
growth. Interrupting this intercellular tit-for-tat causes the neuron to
wither away.
"First we need to
figure out at a molecular level how App works in Down syndrome," said
Mobley. "Then we need to examine other genes that might be involved and
test possible compounds in mouse and human cells. If we are able to do
all that, we might begin to think of helping children and adults with
Down syndrome to develop and age more normally."
The research is
published in the to July 6 issue of Neuron
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