Study Of Molecule Transporters During Stroke Offer Clues Into Possible Therapies, Colorado State Researcher Finds
Wednesday, November 27, 1996
FORT COLLINS--Why do nerve cells die during stroke? A
Colorado State researcher believes the culprit may be in the
performance of certain molecule transporters during an attack.
The preliminary findings by James Madl, associate professor
of anatomy and neurobiology, are part of a two-year study
searching for possible new therapies to minimize brain damage
after a stroke has occurred.
"The potential exists for greatly decreasing permanent
damage induced by stroke," Madl said. "After a stroke occurs, we
may have hours, possibly days, to prevent damage from spreading
beyond the core of the stroke-damaged area."
Madl's research has focused on two main types of molecule
transporters that appear to work against each other during
stroke, leaving excessive amounts of signaling molecules like
glutamate in the brain.
During a stroke, nerve cells in the brain run out of energy
due to a lack of oxygen and nutrients carried by blood. When
nerve cells run out of energy, some of their transporters can"t
remove some of these signaling molecules, including glutamate.
This excites nerve cells at a time when they have little energy,
causing further damage.
Some of these transporters protect the brain by removing
some of the excess glutamate from the area where the stroke
occurs.
However, Madl's study shows there is a lack of these
protective transporters when there is also increased acid, or pH,
in the blood. In stroke victims, glucose converts into lactic
acid, which causes increased acidity. Previous research has shown
that increased acidity is linked to increased stroke damage, Madl
said.
"Perhaps a combination of loss of energy during stroke and
high acidity may be affecting these protective transporters,
which are key to preventing further damage in the brain," Madl
said.
Madl's research also points to the existence of one or more
transporters that reverse themselves during a stroke and dump
their glutamate cargo. The protective transporters cannot remove
all the excess glutamate, which opens the door to further damage
of cells surrounding the stroke's epicenter.
The next step in Madl's research is to further analyze the
transporters that reverse themselves and find out what triggers
that response. That discovery, says Madl, could lead to the
creation of a drug treatment that would isolate the ineffective
transporters and prohibit them from discarding glutamate.
"Past research has focused on blocking the effects of
glutamate once it has been released," Madl said. "By
understanding these transporters, we may find ways to block the
release of glutamate altogether, which would result in a smaller
damage area," Madl said.
Finding treatments after the fact could have a dramatic
impact on the success of rehabilitation in stroke victims.
According to the American Heart Association, stroke is the
third leading cause of death in the United State, behind heart
disease-related deaths and cancer. Stroke also is the leading
cause of disability nationwide, claiming 500,000 victims every
year.
Madl's research is funded by a one-year, $20,000 grant from
Colorado State's College of Veterinary Medicine that ends in
June. An additional $57,074 grant from the American Heart
Association will fund the studies through June 1998.
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