Contact: Jeffrey Kuret, Ph.D., (614) 688-5899
Written by Darrell E. Ward, (614) 292-8456 [email protected]
CHEMICAL MARKER FOUND FOR BRAIN DAMAGE IN ALZHEIMER'S DISEASE
COLUMBUS, Ohio -- Scientists have identified a common
molecular marker for three major lesions found in brains of
people with late-stage Alzheimer's disease.
The finding could lead to a better understanding of how
Alzheimer's disease progresses. In the future, it also
could serve as a biochemical marker to help diagnose or
stage the disease, and determine the effectiveness of new
treatments.
"For the first time, we have established a common
denominator among the three major types of damage that arise
in the brain during Alzheimer's disease," said Jeffrey
Kuret, associate professor of medical biochemistry at Ohio
State University.
"This will give us information about how this damage occurs
and perhaps what pathway is involved in its development."
The study, which involved a team of researchers led by
Kuret, appears in the October issue of the American Journal
of Pathology.
It is a follow-up of earlier work that first suggested the
association of high levels of three key enzymes with
Alzheimer's tissue in the test tube.
The present study confirmed that high levels of the enzymes
are also associated with damaged neurons in thin slices of
intact brain tissue from people who died of Alzheimer's
disease.
The three enzymes belong to the casein kinase-1 family of
enzymes. One of the enzymes, the delta kinase, was present
in Alzheimer's patients at levels more than 30 times that
found in brain tissue from aged-matched controls.
As predicted from their earlier work, the researchers found
all three enzymes associated with two types of lesions known
as neurofibrillary tangles and neuritic plaques.
"The real surprise came when we also found high levels of
the enzymes in a third type of lesion, called
granulovacuolar degeneration bodies," said Kuret. "This was
a complete surprise."
It was also an important surprise.
"This is the first molecular marker for granulovacuolar
degeneration bodies," he said. "Until now, there has been
no reliable molecular tag that enabled scientists to purify
these bodies and study their composition."
A major problem in Alzheimer's research is trying to
understand how the three types of cellular damage occur, and
how they are interrelated," he said.
"The presence of high levels of casein kinase enzymes might
reflect a common pathway in the generation of these
lesions."
Next, Kuret will look at casein kinase levels in other
neurodegenerative diseases. He also plans to study the
genetic control of the enzymes to understand why they are
present at such high levels.
Funding for this research was provided by the National
Institutes of Health and the Alzheimer's Association. The
work also involved researchers from Northwestern University
Medical School; Nathan Kline Institute for Psychiatric
Research, Orangeburg, New York, the ICOS Corporation,
Botbell, Washington; and Rush-Presbyterian-St. Luke's
Medical Center, Chicago, Illinois.
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