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Nerve Cell 'Traffic Jam' May Trigger Alzheimer's

Neural clogs appear much earlier in disease than thought

THURSDAY, Feb. 24, 2005 (HealthDay News) -- Like cars backed up on a freeway, blockages in nerve cell signals may lead to the neurological traffic jam that is Alzheimer's disease, researchers say.

The research is preliminary, but a new study in mice suggests this type of neural backup occurs much earlier in the disease than previously thought. It may also help trigger the buildup of beta amyloid protein plaques that is the hallmark of Alzheimer's, the researchers believe.

The findings "point out that this transport system [nerve cell signaling] gets disrupted in Alzheimer's," explained Dr. Bill Thies, vice president of medical and scientific affairs at the Alzheimer's Association.

"The researchers propose that it's this disruption that ultimately triggers the amyloid buildup," he said.

While he labeled the findings "outstanding science," Thies cautioned that this remains just one of many theories as to the exact cause of Alzheimer's. He also stressed that any therapies based on these findings remain years away.

Reporting in the Feb. 24 issue of Science, researchers at the University of California, San Diego (UCSD) focused their efforts on axons -- long, skinny neural highways that pass biochemical messages between nerve cells throughout the body.

Scientists have long observed that axon blockages are a characteristic feature of late-stage Alzheimer's. However, the UCSD team say they have now spotted these globular axonal "defects" in mice more than a year before the rodents develop Alzheimer's-like symptoms.

Their early appearance now points to axon blockages as a potential cause, not effect, of the brain-robbing illness, they say.

The findings yielded another intriguing possibility. In Alzheimer's, the buildup of amyloid plaques within brain tissue is accompanied by a second aberration -- the accumulation of neurofibrillary 'tangles' composed of another protein, called tau.

Tau is also "a protein that appears to regulate traffic within axons," study senior author Lawrence S.B. Goldstein noted in a written statement. That suggests these tau-related blockages within axons "may promote the generation of excess amyloid beta, the protein in amyloid plaques," he said.

According to Thies, "people have been trying to figure how plaques and tangles fit together" in Alzheimer's for a long time. While many believe amyloid deposits lead to tau tangles, others suspect it works the other way around. "There's still no agreement," he said.

"But this paper suggests that axon transport [blockage] is critical in creating amyloid," Thies said. "So, if you correct the tau problem in the axons, you'll correct the amyloid problem."

Unfortunately, no safe, effective agents to untangle this transport mechanism exist, Thies said, partially because most pharmaceutical companies continue to focus on amyloid in their search for effective Alzheimer's drugs.

Right now, Thies said, research into ways to fix impaired tau transport "is on the cutting edge of what people are working on."

"So, this is not going to be in your drugstore tomorrow," the Alzheimer's expert stressed. "It's really outstanding science, but how it fits into the overall picture of trying to treat the disease -- that's still in the offing."

Still, he said this and other discoveries should give patients with Alzheimer's -- and their loved ones -- real reason for hope.

"Alzheimer's is a reasonably complex disease hitting the most complex organ in the body, so we're going to have to know a lot about it," Thies said. "But the fact is that, right now, there are a tremendous number of potential new agents out there."

"We have so many potential pathways, and some of them are going to get us through to the other side," Thies said. "To me, that's the biggest reason for enthusiasm."

More information

For more on the potential causes of the disease, head to the Alzheimer's Association.

SOURCES: Bill Thies, M.D., vice president, medical and scientific affairs, Alzheimer's Association; statement by Lawrence S.B. Goldstein, Ph.D., Department of Cellular & Molecular Medicine, University of California, San Diego; Feb, 24, 2005, press release, University of California, San Diego; Feb. 24, 2005, Science
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