Certain proteins may slow the devastating memory loss caused by Alzheimer’s disease, according to a groundbreaking Iowa State University study.
Auriel Willette, a researcher in food science and human nutrition, found evidence that an elevated presence of a protein called neuronal pentraxin-2 may slow cognitive decline and reduce brain atrophy in people with Alzheimer’s disease.
Willette will present his findings at the Psychoneuroimmunology Research Society‘s annual scientific meeting, June 3 to 6 in Seattle.
The Alzheimer’s Association predicts that by 2050, nearly 14 million Americans over 65 will have Alzheimer’s. Caring for them will cost an estimated $1 trillion every year.
“It’s just a devastating illness,” Willette said. “Unlike a lot of other neurological diseases, Alzheimer’s disease basically robs you of yourself.”
A groundbreaking study
Researchers have long suspected that inflammation in the brain leads to the cell death and brain atrophy found in people with Alzheimer’s disease. Yet previous studies didn’t place much emphasis on the varying roles of different immune proteins and how they might change the brain over time.
As part of his latest research, Willette analyzed data from the Alzheimer’s Disease Neuroimaging Initiative, an effort to collect and archive brain images and spinal fluid samples for researchers.
He compared brain scans, as well as fluid from the brain and spine, from three groups: people without Alzheimer’s disease, people with mild cognitive impairment or memory problems who may have Alzheimer’s disease, and people with full-blown Alzheimer’s disease.
Willette found that participants with higher levels of neuronal pentraxin-2, the protein that regulates immune function and connections between neurons, showed little or no memory loss after two years. He also found that participants with higher levels of inflammatory proteins in their cerebrospinal fluid showed modestly greater memory loss and brain atrophy over two years.
Neuronal pentraxin-2 is naturally produced in the body, primarily by neurons — nerve cells that carry electrical impulses and chemical signals. The protein seems to be involved in forming or reconfiguring connections between neurons, possibly by clearing away old debris or inefficient connections to make way for new connections.
Willette compared neuronal pentraxin-2 to a chemical bulldozer, clearing away old buildings to make way for new buildings.
“If you have high levels of this synapse-building, inflammation-regulating protein, you may not have as much, if any, change in your memory,” he said.