Recently, researchers began developing a potential therapy for concussions, using an FDA-approved drug that helps reduce the harmful effects of swelling. Specifically, they found that the expression of a certain membrane protein called aquaporin-4 increased dramatically after a head injury and caused damage.
While work on that project continues, other experts believe that aquaporin-4 may be a prime target for Alzheimer’s research. A study conducted by researchers from Oregon Health & Science University has revealed a connection between the protein and possible prevention of the brain disease. While it may not materialize into a lasting cure, the researchers believe that their work could contribute to future therapies and prevention strategies.
"It suggests that aquaporin-4 might be a useful target in preventing and treating Alzheimer's disease," said Dr. Jeffrey Iliff, senior author of the study. "However, we aren't under any illusion that if we could just fix this one thing, then we'd be able to cure Alzheimer's Disease."
In a broad sense, Alzheimer’s isn’t a disease that happens all at once – it takes time and is much more progressive. There is currently no cure for it, but several therapies have been developed that may be effective in slowing it down; the researchers believe that aquaporin-4 could provide another.
Aquaporin-4’s functions as part of the brain's glymphatic system. Under certain conditions, it is the protein that allows cerebral-spinal fluid to enter the brain and wash away other proteins like amyloid and tau – the build up of which are main drivers of Alzheimer’s.
The researchers believe that when the system regulating aquaporin-4 breaks down, amyloid and tau are allowed to build up unchecked, leading to nerve damage. They tested this theory by analyzing three groups of 79 donated brains – people younger than 60 with a history of Alzheimer’s, people younger than 60 without a history of any neurological disease, and people over 60 without Alzheimer’s.
They found that aquaporin-4 levels were well organized and ordered in the brains of people without Alzheimer’s or a history of neurological disease, but older brains with Alzheimer’s had very disorganized aquaporin-4 levels. The researchers posit that Alzheimer’s may have developed in these brains due to decreased function to clear away harmful proteins.
Last year, the researchers were given a $1.4 million grant from the Paul G. Allen Family Foundation to continue their research and develop new imaging techniques that could capture brain processes as they happened. The team’s full study has been published in JAMA Neurology.