Kyla Berrier was in middle school when her family first began to notice her grandmother didn’t have the memory she used to.
“It’s not just the person who has Alzheimer’s that is affected, but the entire family,” said the 22-year-old first-year doctor of nursing practice student.
Now, with a recent $7.7 million grant awarded over the next five years to UF through the National Institutes of Health for Alzheimer's disease research, Berrier said she thinks any progress is beneficial.
This money will allow researchers to expand upon ongoing research to find therapies to treat Alzheimer’s disease.
“It gives us more flexibility and more opportunities to perform larger scale experiments,” said Yona Levites, assistant professor in the Department of Neuroscience at the Center for Translational Research in Neurodegenerative Medicine at UF.
There currently are no treatments that can cure or reverse Alzheimer’s, Levites said.
Researchers reason that previous drugs were tested too late in the disease’s progression, and the patients were beyond the point of return, she said.
Paramita Chakrabarty, a UF neuroscience assistant professor, said the available treatments could extend life by six months.
For this project, the UF researchers will be collaborating with the Mayo Clinic Florida and the Institute for Systems Biology in Seattle, using data collected from both humans and mouse models, according to a news release.
The research will focus on the role the immune system plays into the disease’s development, and researchers hope to use the brain’s innate immune system to modify the pathology of Alzheimer’s disease, Chakrabarty said.
They are working with versions of a few immune genes, which are used in therapies for peripheral immune diseases such as arthritis.
A few pathological identifiers commonly found in patients after death are amyloid plaques, located outside of brain cells, and intracellular tau tangles, Chakrabarty said.
Normally, the amyloid peptide is broken down, but researchers don’t know why it sometimes begins to accumulate in the brain, Levites said. Researchers believe the presence of both the amyloid plaques and tau tangles eventually lead to cell death, which causes the noticeable symptoms, Chakrabarty said.
She said a goal is to find a way to cause the blocks to form at a slower rate or not at all, which might not treat the disease, but it would lengthen the time a person has in a nondemented state.
“We can test proposed genes of interest that came out of the large studies,” Levites said, “and test one-by-one the effect in the models.”
A version of this story ran on page 3 on 9/24/2013 under the headline "UF gets grant to research Alzheimer's"
