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.