A Purdue University researcher has identified a potential therapeutic target for Alzheimer's disease.
Researcher Sandra Rossie, a professor of biochemistry, found that the amount of an enzyme present in neurons can affect the mechanism thought to cause cell death in Alzheimer's disease patients and may have applications for other diseases such as stroke and heart attack.
She revealed that increasing the amount of protein phosphatase 5, or PP5, in rat neural cells resulted in less cell death associated with reactive oxygen species, which chemically damage cell molecules.
Conversely, decreasing PP5 caused greater cell death.
It is known that the cause of Alzheimer's is that overproduction of certain forms of amyloid beta protein by neurons leads to the generation of reactive oxygen species, which activate stress pathways.
"If stress pathways remain active for a prolonged period, the cell will die," said Rossie.
The study showed that PP5 overexpression prevents neuronal death by amyloid beta and shuts off the stress pathways.
When reactive oxygen that wasn't created by amyloid beta was used on the cells, the results were the same. In contrast, neurons with reduced PP5 are more sensitive to death caused by amyloid beta.
"That suggests to us that PP5 protects neurons from cell death induced by reactive oxygen species, not just the presence of amyloid beta," Rossie said.
"This means that PP5 may protect against other health problems involving reactive oxygen species as well, such as stroke and heart attacks," the expert added.
The results are published in the early online version of The Journal of Neurochemistry.