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Assistant Professor James
Lee and his colleagues are researching what causes Alzheimer's
Disease.
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Enzyme
Associated With
Alzheimers’ Identified
By Bryan Daniels
In a recent study, researchers at the University
of Missouri-Columbia identified an enzyme that is responsible
for the deterioration of brain function for people with Alzheimer's
disease. The study was published in the Oct. 25 edition of the
Journal of Neuroscience.
James
Lee, assistant professor of biological engineering in the
College of Engineering,
and his former doctoral student, Donghui Zhu, currently a post-doctoral
research associate at Columbia University, conducted their research
in collaboration with Grace Sun, professor of biochemistry and
pathology and anatomical sciences in the MU
School of Medicine and College
of Agriculture, Food and Natural Resources. Sun also directs
an Alzheimer's project at MU funded by the National
Institutes of Health.
The research team's work focused on amyloid-beta
peptide, a common neuron-killing toxin found in the brains of
Alzheimer's patients, and astrocytes, which support neurons and
are the major cell in the brain. In lab tests, they studied how
the toxin affects and interacts with the cell to activate a critical
enzyme — phospholipase A2. Lab tests showed that with increased
activity, phospholipase A2 negatively affected the mitochondria,
which are responsible for energy production, resulting in increased
oxidative stress. Zhu and Lee said an increase in oxidative stress
further promotes neuron death, worsens the disease and causes
decreased energy levels.
“It's an important aspect in the development of Alzheimer's disease,” Zhu said.
An increase in oxidative stress, Lee said,
is one of the characteristics found in the brains of Alzheimer's
patients. Zhu and Lee hope their findings lead to a medical breakthrough
and the design of effective drugs to treat people living with
the brain disorder that gradually destroys memory and an ability
to communicate and carry out daily activities.
“Alzheimer's is a complicated disease,” Lee said. “We know that phospholipase A2 is one of the key factors. If we can regulate phospholipase A2, maybe it can become part of the therapeutic strategy for treating Alzheimer's.”
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Last Update:
March 12, 2007
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