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Study Puts 1 Alzheimer's Theory in Doubt

Results in mice suggest a key gene might not be to blame, researchers say

MONDAY, Aug. 20 (HealthDay News) -- Research with mice is poking holes in a prevailing theory on the origins of Alzheimer's, scientists say.

Mice without a gene thought to rein in cell-damaging free radicals actually had fewer Alzheimer's-linked brain plaques than mice with the gene.

"This finding may go beyond Alzheimer's into all aging theory," noted lead researcher Carlos T. Moraes, an associate professor of neurology and cell biology and anatomy at the University of Miami Miller School of Medicine.

The study is published in this week's early edition of the journal Proceedings of the National Academy of Sciences.

Moraes said that, right now, "nobody knows what causes Alzheimer's disease," which affects more than 4.5 million Americans according to the National Institutes of Health.

However, one leading hypothesis is that there is a defect in the mitochondrial energy production system in cells, Moraes explained. The mitochondria are the cell's "power houses," giving it the energy it needs to function.

In prior studies, examination of the brain cells of people with Alzheimer's found some defects in an enzyme produced by the cytochrome c oxidase (COX) gene, which is important for mitochondrial energy production.

In addition, so-called "free radicals," which cause oxidative stress, are produced in the cell's mitochondria, Moraes noted. "It was assumed that when you have a problem with the COX gene, you have more free radicals being formed," he said.

To see how the gene worked, Moraes's group removed the COX10 gene in mice engineered to develop Alzheimer's disease.

"We expected to see that these animals would have more amyloid plaques," Moraes said. "But we got the opposite result," he said.

The animals without the COX10 gene actually developed fewer brain plaques than those with the gene, Moraes said. "Those animals also had less free radicals," he said.

The findings suggest that a defect in the COX10 gene develops after amyloid plaques develop, not the other way around, as has been thought, Moraes said.

"The mitochondrial defect in Alzheimer's disease appears to be a consequence of amyloid accumulation, not the cause of amyloid accumulation," he said. "Also, if you have a defect in the COX gene, you are not necessarily going to have more free radicals being formed," he added.

According to Moraes, the finding could have implications for scientists' understanding of the aging brain in general, not just Alzheimer's.

If the findings are duplicated in other research, they might be useful in developing new treatments for Alzheimer's -- treatments that target the COX gene, Moraes said.

One expert agreed that the findings shed new light on Alzheimer's disease.

"This study shows that a genetic manipulation that reduced the activity of a key energy-producing enzyme also reduced free radical damage and Alzheimer pathology in a mouse model," said Greg M. Cole, a neuroscientist at the Greater Los Angeles VA Healthcare System and associate director of the Alzheimer's Disease Research Center at UCLA's David Geffen School of Medicine.

"The results are consistent with other evidence that reducing free radicals can limit Alzheimer amyloid plaque pathology," Cole added. "Examples include reducing caloric intake or increasing antioxidant intake. So, even though clinical trials to treat Alzheimer's with [antioxidant] vitamin E have been disappointing, earlier and more effective reduction of free radical damage could mimic the success of this genetic approach and should still be pursued," he said.

More information

For more on Alzheimer's disease, visit the Alzheimer's Association.

SOURCES: Carlos T. Moraes, Ph.D., associate professor, neurology and cell biology and anatomy, University of Miami Miller School of Medicine, Florida; Greg M. Cole, Ph.D., neuroscientist, Greater Los Angeles VA Healthcare System, and associate director, Alzheimer's Disease Research Center, UCLA David Geffen School of Medicine, Los Angeles; Aug. 20-24, 2007, early edition, Proceedings of the National Academy of Sciences


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