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 actua