Dr. Matthew Parsons has always been interested in how the brain forms and holds memories.
After all, our identities depend on the memories we form over our lifetime. But for people with Alzheimer’s disease, those memories get interrupted.
“A lot of research we do in the lab actually aims to understand how the healthy brain strengthens its connections in such a way that can underline memory formation,” said Dr. Parsons, an assistant professor of biomedical sciences at the Faculty of Medicine.
It’s why he studies the cognitive side of diseases like Alzheimer’s.
Specifically, his focus is a toxic protein that accumulates in the brains of Alzheimer’s patients called amyloid beta. Many think that amyloid beta buildup contributes significantly to the cognitive decline associated with Alzheimer’s disease, although researchers still don’t know precisely what this toxic protein does to our brain cells.
That’s where Dr. Parsons comes in.
As he explains it, brain cells are constantly talking to each other by releasing chemicals known as neurotransmitters.
The strength of this communication is affected by a variety of factors, including the amount of neurotransmitter released from one brain cell and the amount of receptors on a neighbouring cell that can recognize that neurotransmitter.
“Our brain cells have the ability to change the strength of their connections; otherwise we would be robots where a certain input always generates the same, predictable output,” he noted. “But we are not robots, and our actions are shaped by prior experiences and our memories.”
To form these memories, our brain cells need to be able to change the strength of their communication.
Although it’s known that amyloid beta impairs the brain’s ability to strengthen its connections, how it does so is less clear.
“In order to find more effective treatments for Alzheimer’s disease, we need to understand the disease at so many levels.”
Dr. Parsons wants to understand the effect that amyloid beta has on neurotransmitters and receptors and why brain cells are less able to strengthen their connection when amyloid beta is present.
“In order to find more effective treatments for Alzheimer’s disease, we need to understand the disease at so many levels; from the behaviour of cells in a dish all the way up to clinical trials in Alzheimer’s disease patients, and everywhere in between,” he said.
“I don’t think it’s a coincidence that a wide variety of different neurodegenerative diseases, with completely different environmental and genetic contributing factors, can all be associated with a loss of cognitive function,” Dr. Parsons continued. “Our strategy is to take what we have learned about how a healthy brain forms memories and then examine how these mechanisms work, or fail to work, in diseases such as Alzheimer’s.”
Through his research, Dr. Parsons hopes to shed new light on our understanding of the debilitating cognitive impairments in Alzheimer’s disease and help identify new strategies to improve it.
Dr. Parsons, a three-time Memorial alumni (B.Sc.(hons.)’03, M.Sc.’06, PhD Distinction ’11), recently received $225,000 from the Alzheimer Society Research Program as part of its new Investigator Grants for the project.