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UCLA researcher discovers the role of common painkillers in protecting against Alzheimer's disease
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 plaque formation.
"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.