Watching Changes In Alzheimer's Brain

Armen Hareyan's picture

It is known that brain injuries lead to increased risk for Alzheimer's disease. To clarify the links, researchers watched how brain changes after an injury.

The protein - amyloid beta - was found to be associated with Alzheimer's disease in a study conducted in 2005. Disease sufferers experience difficulties in brain cell communication, which is found to be directly linked to amyloid beta - cell communication reduction was associated with protein decrease.

A joint team of researchers from Washington University School of Medicine in St. Louis and the University of Milan examined 18 patients who suffered 'traumatic brain injuries or ruptured brain aneurysms' and were receiving appropriate treatment to recover. While the patients were being treated in intensive care unit, researchers got permission from their family members to take samples of brain cells. The samples allowed to understand how fluid between brain cells develops and how it is associated with neurological disorders.

"Proving that we can directly measure amyloid beta in the human brain is an important step forward for both clinical and basic research, and that may be true not just in Alzheimer's disease but also in other serious neurological disorders," says co-first author David L. Brody, M.D., Ph.D., a Washington University neurologist who treats brain injury and general neurology patients at Barnes-Jewish Hospital.


Researchers were suggesting a thesis that brain injuries increase amyloid beta levels, which increases risk for Alzheimer's disease, and they were seeking to prove this thesis. However, this trial came with a controversial finding - not injury, but the process of recovering from the injury, causes increase in amyloid beta levels. This means that the better one's neurological status is, the higher protein levels are.

Now researchers are considering the link between brain injuries and Alzheimer's disease to identify better treatment methods for injuries, which will cut Alzheimer's risk for a long period of time.

"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 David L. Brody, a Washington University neurologist. "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."

"The results have potentially important clinical implications because the measurement of amyloid beta in the human brain may turn out to be a good indicator of how well brain cells are communicating with each other, even in very sick patients," says senior author David M. Holtzman, M.D., the Andrew B. and Gretchen P. Jones Professor and head of the Department of Neurology at Washington University. "If the results are validated in further studies, this may assist physicians in making important patient management decisions in patients with acute neurological disorders."

The research has set its ultimate goal as to provide treatments and means of intervention against traumatic brain injury to prevent the long term risk of Alzheimer's disease.