Scientists in an attempt to find out why brain injury is linked to Alzheimer’s are measuring the ebb and flow of a substance in the brain known to cause the disease. Researchers from Washington University School of Medicine in St. Louis and from the University of Milan to find this link are peeping into the brains of people suffering severe brain injuries. The study is to be published in the August 29 issue of Science and researchers hope by understanding why brain injury increases the risk of developing dementia in later life they could subsequently find a way to lower the risk.

"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 lead researcher Dr. David Brody, a neurologist at Washington University in St. Louis.
Increased amounts of a protein called beta-amyloid, best known for causing plaques in the brains of people with Alzheimer’s disease was said to be the culprit.
Beta-amyloid is a normal component of the brain, but scientists do not really know what it does. Researchers were prepared to see the beta-amyloid levels raised in people with brain injuries, and the levels reducing as they recovered. The researchers reported the results to be the opposite, the beta-amyloid levels increased as the patients improved and reduced as they worsened.

"Our study is just the beginning," Brody said. "Amyloid-beta measurements in the brain may turn out to be a good indicator of how well the cells are communicating with each other.'

Beta-amyloid is found in soluble forms in the fluid that bathes the brain and scientists do not know what makes it form the typical plaques in Alzheimer’s patient’s brains. Neither do they know why brain trauma often results in Alzheimer’s later in life. One theory that is being studied is the possibility that the excess beta-amyloid speeds up any dementia forming that is present in the brain. Some experts feel it could be as the injury decreases a person’s cognitive reserves and the symptoms are apparent sooner.

A process called intracerebral microdialysis, already undertaken on mice by Washington University, where a minute tube would be inserted into the brains of people as they underwent surgery to allow measuring of beta-amyloid fluid levels on an hourly basis was undertaken. Dr. Sandra Magnoni of the Ospedale Maggiore Policlinico, a major trauma center in Milan that has experience with the technique and Brody joined forces. They took permission to perform the procedure from the families of patients suffering brain injuries from car crashes, falls or hemorrhages from burst blood vessels and eighteen said yes.

Once the catheter was placed in patients' brains, it stayed there for three to seven days while ICU doctors and nurses otherwise provided routine care. They kept track of the patients' neurologic changes with a standard tool called the Glasgow Coma Score while Brody tracked the beta-amyloid levels. He found these mirrored the coma score, with a direct relationship to each patient's neurological status. The results matched the findings from their earlier research on mice.

Dr. Ramona Hicks, a specialist in traumatic brain injury at the National Institutes of Health, which helped fund the work, said it’s important as so much Alzheimer’s research must be performed on animals.

The recent research may not have answered all the questions but it has helped researchers with a valuable new tool for studying both Alzheimer's risk and just what happens during brain-injury recovery. "It sort of sets a platform for future studies," said NIH's Hicks.  “This study raises more questions than it answers,” Brody says. “It’s really just the beginning.”