Alzheimer's Drug May Help Preemies
Namenda May Help Prevent Brain Damage in Premature Infants
By
Jennifer Warner
WebMD Health News
Reviewed By
Louise Chang, MD
June 24, 2008 — A drug used to treat older patients with Alzheimer's disease may help
protect the youngest premature infants from harm.
A new study suggests that Namenda, a drug originally developed to treat
Alzheimer's disease, may help break the cycle of brain damage many premature
infants face.
Researchers found that rats treated with Namenda suffered less brain damage
after a loss of oxygen and blood supply to the brain, a common problem in
premature infants because of underdeveloped organs.
These findings are only preliminary and must be replicated in humans, but
researchers say the results may offer a new avenue for treating and potentially
preventing brain damage among premature infants. No such treatment exists.
Protecting Premature Brains
An increase in the number of multiple births has led to a
rise in the number of premature births in the U.S. Although advances in
medicine have meant improved survival rates for most premature infants, up to
35% of premature infants suffer from lasting brain damage, which can lead to
learning difficulties and conditions like cerebral palsy.
Researchers say the problem in developing treatments to prevent brain damage
in premature infants is that the premature brain behaves very differently from
the adult brain.
"The premature brain is not just a 'small' adult brain — it is
physiologically different and thus contains unique targets for therapy,"
says researcher Frances Jensen, MD, of Children's Hospital Boston, in a news
release.
Jensen says a loss of blood and oxygen to the brain appears to act upon
brain cells known as oligodendrocytes in the premature brain. Immature forms of
these cells are particularly vulnerable to damage during development.
Namenda Targets Vulnerable Brain Cells
In this study, published in the Journal of Neuroscience, researchers
first confirmed the presence of NMDA receptors in premature brains of humans as
well as rats. NMDA receptors are targeted by Namenda.
Then researchers tested the effects of a loss of oxygen and blood supply on
oligodendrocytes treated with Namenda. Without treatment, the loss of blood and
oxygen supply triggered an over-activation of the NMDA receptors, leading to
brain damage and loss of white matter.
But when rat pups were treated with Namenda after the episode, the rats
suffered less immediate and long-term injury.
Researchers say the next step will be to evaluate the potential safety risks
of treating newborns with Namenda and conducting clinical trials.
SOURCES: Manning, S. Journal of Neuroscience, June 25, 2008; vol 28. News release, Children's Hospital Boston.
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