Scientists Track Hourly Changes in Alzheimer's Protein
THURSDAY, Aug. 28 -- A group of researchers has described hourly changes in a protein in the brain that is thought to play a key role in Alzheimer's disease.
In a 2005 study, the protein, known as amyloid beta, was directly linked to brain cell communication in a mouse model of Alzheimer's disease. When brain cell communication increased, so did amyloid beta. When there was reduced communication, amyloid beta decreased.
In the new study, published in the Aug. 29 issue of Science, researchers from Washington University School of Medicine in St. Louis and from the University of Milan sought to find out why brain injury is linked to a higher risk of developing Alzheimer's disease.
For their study, the researchers took samples of the fluid between the brain cells of 18 patients who were recovering from traumatic brain injuries or ruptured brain aneurysms. The samples were taken while the patients were in the intensive care unit, with the permission of their families.
The researchers didn't find what they expected. Having hypothesized that brain injuries would lead to an increase in amyloid beta levels, the researchers actually found that recovery from brain injury -- not the injury itself -- was associated with increased amyloid beta. In other words, the better the patient's overall neurological status, the higher his or her amyloid beta levels.
"We can't at this point rule out a very early spike in amyloid right after a brain injury," co-first author David L. Brody, a Washington University neurologist who treats brain injury and general neurology patients at Barnes-Jewish Hospital, said in a school press release. "This study is just the beginning."
More studies are needed to find out why brain injury increases Alzheimer's risk.
In addition to the possibility that brain injury accelerates harmful processes that cause Alzheimer's disease, another potential explanation for the link between brain injury and Alzheimer's is that the injury may reduce the brain's ability to compensate for Alzheimer's-related damage, making the symptoms appear earlier than they would otherwise.
"We haven't measured how brain injury affects amyloid beta inside cells, nor have we determined whether brain injury affects the ability of amyloid beta to form small aggregates that may be especially harmful," said Brody. "Our ultimate goal is to develop interventions that we can apply after a traumatic brain injury to improve outcomes and reduce the long-term risk of Alzheimer's."
Posted: August 2008