Illinois State University’s Nathan Mortimer received a nearly $300,000 grant from the National Institutes of Health (NIH) to understand the connection between the immune system and Alzheimer’s disease.
The two-year grant from the NIH’s National Institute on Aging totals $293,000, and will support efforts in Mortimer’s research lab to examine a protein called amyloid beta (A-beta) that is thought to accumulate in the brains of Alzheimer’s patients.
Nathan Mortimer
“A-beta is a little peptide that gets made in your body,” said Mortimer, who is an assistant professor of cellular immunology in the School of Biological Sciences. “One of the big questions in the field is what is A-beta and why is it there? If it only exists to build up into plaques, which can interfere with normal function and cause Alzheimer’s disease, why would it last through millions of years of evolution?”
According to Mortimer, a large part of the NIH grant will go to gaining a better understanding of how A-beta functions within the immune system. That knowledge could arm neurobiologists with information about the connection between the immune system and inflammation in the brains of Alzheimer’s patients. “The question of how the immune response influences disease progression is a fairly new area in Alzheimer’s research,” said Mortimer. “We’re hoping to add a piece to that puzzle for researchers.”
Mortimer and his team of undergraduate and graduate students believe A-beta plays a role in the body’s “innate” immune system. Unlike an acquired immunity, which produces antibodies to fight infection, innate immunity is the body’s first line of defense and identifies something as foreign through a series of receptors. “We’ve maintained innate immunity through every stage of evolution, but it is still understudied,” said Mortimer.
The immune cells recognize A-beta, and that’s why it can trigger a response. — Nathan Mortimer
In order to explore the possible connection, Mortimer’s team works with an insect that only possesses an innate immune response—the fruit fly, Drosophila melanogaster. When A-beta was removed from flies, the team found they could not develop an immune response to infection. Even more telling, when human A-beta was placed in the fly, it led to development of an auto-immune disease. “The cells started attacking the tissue in response to human A-beta,” said Mortimer. “This means the immune cells recognize A-beta, and that’s why it can trigger a response.”
The grant will also fund the work of a doctoral student in the Mortimer lab, who will look at a parasite that has managed to somehow block the interaction of A-beta and the immune system altogether. Mortimer has long worked with the parasitoid wasps that infect flies in his studies of the host-parasite system. Yet when introducing A-beta to the equation, the parasitic wasps—which are so tiny they cannot even sting a human—appear to shut down the interaction between A-beta and the immune system. “We’ll be looking at how the parasitoid wasps evade the immune system and interfere with A-beta,” said Mortimer.
