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NSAIDs May Help Brain Heal Itself

Reducing inflammation lets new neurons develop

THURSDAY, Nov. 13, 2003 (HealthDayNews) -- Two studies shed new light on the role of brain inflammation in diseases such as Alzheimer's and other dementias.

The results of both studies indicate that treatment with nonsteroidal anti-inflammatory drugs (NSAIDs), which include aspirin and other aspirin-like drugs, can restore brain cell (neuron) production and lower levels of beta-amyloid by reducing inflammation.

In one study, which appears in the Nov. 14 issue of Science, Dr. Steven Paul and researchers from the drug maker Eli Lilly and Co. report that anti-inflammatory drugs can reduce the production of amyloid-beta, including amyloid-beta-42. The buildup of amyloid-beta-42 seems to be the most harmful form of amyloid-beta seen in the brains of Alzheimer's patients.

Paul's team found that a G protein, "Rho," increases amyloid-beta levels as it interacts with another molecule, called "Rock." In experiments in mice, the researchers found NSAIDs blocked the Rho-Rock interaction, lowering brain levels of beta-amyloid.

These results support the notion that NSAIDs have a protective effect against future neurodegeneration, says Dr. Lon Schneider, a professor of psychiatry, neurology and gerontology at the University of Southern California.

However, the exact role of amyloid-beta in Alzheimer's disease is controversial, he adds. In addition, the role that neuron production plays, if any, in preventing dementia is unknown.

Schneider believes trials are needed to see if and which nonsteroidal anti-inflammatory drugs might prevent various types of dementia and treat head injury and stroke.

In the second report, which appears in the Nov. 13 issue of Science online, a team led by Theo Palmer, an assistant professor of neurosurgery at Stanford University, experimented with rats to see the effect reducing brain inflammation might have on neuron production.

"The dogma for many decades has been that the brain doesn't replace neurons, but that is not true. There are regions of the brain that continue to make neurons throughout life. These new neurons are made by stem cells called precursors," Palmer says. These new neurons might be important for memory and learning, he adds.

The team found that in rats in which brain inflammation was induced, the production of new neurons stopped. However, when they treated the rats with the anti-inflammatory drug indomethacin, the production of neurons was completely restored.

These results suggest memory and learning problems seen in conditions such as Alzheimer's and other dementias, stroke and traumatic brain injury might benefit from a simple drug such as indomethacin, Palmer says.

"However, we don't know if that will turn out to be true," Palmer notes. "We also don't know whether making new neurons really plays a functional role in memory and learning."

Dr. John Morris, director of the Alzheimer Disease Center at Washington University, comments, "These reports suggest that commonly used anti-inflammatory drugs may lessen the toxic effects of brain inflammation believed to be important in Alzheimer's disease."

"However, neither study involved human subjects. Whether the positive effects shown in these experimental models translate to actual patients is far from clear," Morris says. "Several clinical trials now under way with anti-inflammatory drugs in older adults eventually should help answer whether these agents are useful in reducing the risk of Alzheimer's."

"Until and unless there are positive results from human trials, no one should take these drugs specifically to treat or prevent Alzheimer's disease, especially in light of the potentially serious side effects of the drugs," he cautions.

More information

To learn more about dementia, visit MedlinePlus. Get an explanation of NSAIDs from the American Academy of Orthopaedic Surgeons.

SOURCES: Theo Palmer, Ph.D., assistant professor, neurosurgery, Stanford University, Palo Alto, Calif.; Lon Schneider, M.D., professor, psychiatry, neurology and gerontology, Keck School of Medicine, University of Southern California, Los Angeles; John C. Morris, M.D., professor, neurology, and director, Alzheimer Disease Research Center, Washington University School of Medicine, St. Louis; Nov. 13 and 14, 2003, Science
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