The damage in the brain caused by Alzheimer's disease is triggered by a protein superstructure-amyloid beta, scientists revealed.
Researchers at the University of California have shown that amyloid beta disrupts one of the brain's anti-oxidant proteins and demonstrates a way to protect that protein, and perhaps others, from amyloid's harmful effects.
"Amyloid seems to cause damage to cells. We have reported in a very detailed way one potential interaction of how amyloid can cause disease, and we found a way to stop it," said Jerry Yang.
Their study focused on catalase-an enzyme that mops up excess oxidants-as catalase normally helps to prevent the kind of damage seen in the brains of patients with Alzheimer's disease and previous work had found catalase proteins deposited within amyloid plaques.
Lila Habib, the first author of the report, added amyloid to cultured neural cells and looked at its effects.
"We were able to determine that amyloid beta and this anti-oxidant enzyme, catalase, interact, and that this interaction harmed catalase so it wasn't able to perform its physiological function: to degrade hydrogen peroxide into oxygen and water," she said.
When Habib coated the amyloid with a small molecule designed to prevent its interaction with other proteins, she was able to restore the activity of catalase and return hydrogen peroxide to normal levels within the cells.
The coating Habib used to probe the interaction between amyloid and catalase is a candidate drug - one of a class of molecules that Yang's lab has developed.
Yang said: "Not only are we learning more about the disease, but we are also developing a potential strategy for treatment that is currently testing the new approach in a mouse model of the disease."
The results would appear in the Journal of Biological Chemistry.