Recent findings by researchers at the School of Medicine has reversed the chronology of events associated with the development of Alzheimer's disease.
A new study led by Pharmacology professor Domenico Pratico found that amyloid plaques -- traditionally believed to contribute to the oxidative stress that causes brain cell death -- actually come after, not before, the oxidation.
According to the scientists, the new finding creates new venues to explore Alzheimer's research.
"This opens a lot of interesting hypotheses for therapeutics," Pratico said in a statement.
Alzheimer's disease, which affects ten percent of Americans over the age of 65, leads to an eventual loss of roughly 40 percent of brain cells. These cells, called neurons, are responsible for coordinating movement, recognizing errors and recalling information. Patients inflicted with Alzheimer's eventually lose memory function.
Although the full spectrum of development for Alzheimer's disease still remains unclear, the researchers base their investigation on one of two main theories.
The first is the development of amyloid plaques, small patches of growth in the brain, which initiate certain proteins to attack neurons, thus leading to brain cell damage.
The second theorizes that the amyloid proteins produce highly reactive molecules, which attack fatty tissue in the brain. When there is a large buildup of these molecules and the brain cannot destroy them, oxidative stress occurs, which eventually leads to cell malfunction and death.
Central to both theories is the view that the amyloid plaque is a factor for the initiation of Alzheimer's. Pratico and his colleagues were able to show that the oxidative stress occurs before amyloid plaque formation by studying the brains of both genetically engineered and normal animals at six developmental stages.
"At seven months, there is a 25 percent more oxidative damage in [Alzheimer's disease] mice than is present in normal mice, and this differential keeps increasing until it is 100 percent or higher at 10 or 11 months," Pratico said. "At 12 months, oxidative damage is 200 percent higher" than in normal mice.
Other neurologists see the significance to the new development as well.
"Oxidative damage can be used as a potential diagnostic clue" Neurology professor Christopher Clark, who has collaborated with Pratico before, said.
"One could pick out markers of oxidative damage in urine so this could provide a potential diagnostic test," Clark said. "Related to this, it offers a potential test for monitoring oxidative damage in the individual, monitoring disease activity."
The study was published in the June 15th issue of The Journal of Neuroscience.
