Noticing the loss of memory in the man who was more like a grandfather to her than a distant relative was the hardest part for Gabriela Rodriguez.
“He passed away after a pretty severe fight with dementia, and toward the end, it was difficult to see,” she recalled.
But out of loss, Rodriguez found inspiration, committing herself to pursuing an academic career that could help solve the mysteries of—and perhaps contribute to—a cure for dementia-related illnesses.
Today, as a Ph.D. student at the University of Miami, she is part of a team led by neuroscientist Oliver Bracko that is studying how a person’s own immune system may be a factor in the progression of neurodegenerative diseases like Alzheimer’s. Pivotal to their research is the study of neutrophils, white blood cells that help the body fight infection.
“We’ve previously shown that neutrophils block blood vessels and contribute to the reduction of blood flow to the brain in mouse models of Alzheimer’s disease,” explained Bracko, an assistant professor of biology. “However, there is a knowledge gap in how and when neutrophils change and become activated and how they may be driving interactions within the network of oxygen- and nutrient-carrying blood vessels to cause neuroinflammation and cognitive impairment.”
With a $3.4 million grant from the National Institute of Neurological Disorders and Stroke (NINDS), the team hopes to bridge that knowledge gap.
Working tirelessly out of a lab in the Department of Biology in the College of Arts and Sciences, Bracko, Rodriguez, and doctoral student Zeynab Tabrizi will employ a process called longitudinal in vivo two-photon imaging to determine how and when neutrophils become reactive and cause inflammation in the brain.
They will also use a single-cell sequencing process to determine whether certain neutrophils become more reactive in disease models and whether disease-associated neutrophil subpopulations drive disease progression. “We will functionally test if neutrophils can be stopped from being activated to slow down disease progression,” Bracko said.
The five-year NINDS study could be one of the few of its kind.
“I believe our study is very novel in some ways,” said Bracko, who has also received funding from the Alzheimer’s Association for other areas of his research. “Our research shows that the immune system is really contributing to damage in the brain. It’s a new concept, but it’s gaining a lot of attention.”
With about 6.9 million Americans aged 65 and older living with Alzheimer’s, and with the Centers for Disease Control and Prevention estimating that the number of people with the illness in the U.S. will double by 2060, the researchers’ work could have important implications for future treatments.
“Dementia-related illnesses like Alzheimer’s are not simple diseases; they’re not only challenging for patients but also for family who take care of those patients,” said Tabrizi, who joined Bracko’s lab last year. “Our research is important because I feel it could contribute to controlling the progression of the disease.”
Rodriguez echoed those sentiments. “There’s so much innovation happening now that I can only describe the feeling as hope,” said Rodriguez, who earned her undergraduate degree in biology and microbiology and immunology from the University in 2023.
“There are not only people suffering from it directly but also those who provide support for individuals with the condition. It’s such a difficult disease because it’s so trying in different ways,” she said. “And although we may not have the solution or the fundamental understanding right now, we’re moving at such a rapid pace in treatment that I hope future generations won’t have to suffer the same way with it and that the disease won’t be seen as a death sentence.”
