"What's interesting is when we studied the brains of people with AD, we saw that, compared to age and gender-matched controls, STI1 levels are increased. We think of this increase as a compensatory response that could protect against insults from this amyloid-β. So we tested it in mouse neurons to see what happens if you increase or decrease the levels of STI1," says Prado, a professor in the Departments of Physiology and Pharmacology and Anatomy and Cell Biology at Western's Schulich School of Medicine & Dentistry. "When we decreased the levels of STI1, the neurons became more sensitive to attack by amyloid-β, and when we increased the STI1, it seemed to mitigate or decrease the toxicity of amyloid-β."

"You have to think of AD as one big puzzle. Every year scientists are putting new pieces in, and now we found that STI1 is one of the pathways in the puzzle," says Prado. "The disease is very complex, but new clues on how we may be able to help the brain to resist the toxins in AD are starting to emerge. We are starting to see the big picture. It may still take years, but we're going to put this puzzle together and find a way to slow down or cure AD."