March 12, 2003
Contact: Rachel Champeau ( email@example.com
In a breakthrough study, UCLA scientists have found
that common painkillers such as ibuprofen and naproxen
may actually dissolve the brain lesions — or amyloid
plaques — that are one of the definitive hallmarks
of Alzheimer's disease. The findings are reported in
the March 31 issue of Neuroscience.
Principal investigator Jorge R. Barrio, professor of
molecular and medical pharmacology at the David Geffen
School of Medicine at UCLA, has used FDDNP, a new chemical
marker developed in his laboratory at UCLA, to visually
zero in on the brain lesions present in Alzheimer's
disease. He discovered that common over-the-counter
pain medications — known as non-steroidal anti-inflammatory
drugs — bind to amyloid plaques, and may help
dissolve existing plaques and prevent the formation
of new ones.
Experts suspect that the amyloid plaques, which the
UCLA chemical marker can measure, disrupt cell function
and kill off brain cells, leading to disorientation
and progressive memory loss.
The UCLA work suggests a possible explanation for epidemiological
observations that people who take anti-inflammatory
medications over several years have a lower risk for
later development of Alzheimer's disease.
"We believe the UCLA observation is extremely
important because early diagnosis of Alzheimer's disease
now has an underlying purpose: early therapeutic intervention
at the stage where brain cell degeneration is minimal.
This would provide hope to patients and families by
modifying outcomes," Barrio said.
During the study, lab researchers took Alzheimer's
diseased brain fibers and added anti-inflammatory drugs
and then the chemical marker, FDDNP, which highlights
the plaques with a fluorescent glow. Researchers found
that the drugs bind to amyloid plaque formations. Additional
test tube studies with the FDDNP chemical marker, synthetic
amyloid and anti-inflammatory drugs showed that the
drugs actually may dissolve the plaques and even inhibit
"This new technology will likely help us monitor
new vaccines and drugs designed to prevent and treat
the brain damage caused by Alzheimer's disease,"
said co-author Dr. Gary Small, Parlow-Solomon Professor
of Aging and professor of psychiatry and biobehavioral
sciences at UCLA.
Previously, the same research group discovered that
positron emission tomography (PET) scans of patients
injected with FDDNP showed the presence of early brain
lesions — before the plaques are believed to destroy
brain cells. If experts' hypotheses about the lesions'
role prove accurate, UCLA's technique could identify
when medical intervention may still stave off or prevent
the onset of the disease.
Barrio adds that the discovery of the painkiller interaction
with the brain plaques will also provide a unique opportunity
to develop new, more efficient drugs designed to destroy
and prevent plaque formation.
Barrio and Small's next step will be to monitor therapeutic
drugs in a group of Alzheimer's patients and compare
results with those of unaffected individuals and patients
with other dementias.
"These studies suggest a previously unsuspected
way in which the non-steroidal anti-inflammatory drugs
may interact with Alzheimer amyloid," said Dr.
John Breitner of VA Puget Sound Health Care System,
Seattle, and the University of Washington.
"They also show that different drugs in this class
may have different effects on amyloid. Clearly, we have
a great deal to learn about the way in which these drugs
may prevent Alzheimer's disease," Breitner said.
"The UCLA work appears to open a whole new avenue
of investigation in this important area."
Alzheimer's disease often begins with mild memory lapses,
then gradually advances to dementia — a progressive
deterioration of memory, language and most mental functions.
Alzheimer's patients eventually become bedridden and
require constant care. The United States spends roughly
$100 billion on the disease per year.
The UCLA study was supported by grants from the U.S.
Department of Energy. Other co-authors include Eric
Agdeppa, Vladimir Kepe, Nagichettiar Satyamurthy, Andrej
Petric, Jie Liu, Greg Cole and Sung-Cheng Huang.