ShareThisShocks to the mind can have equally devastating long-term consequences for the brain as physical trauma, researchers are learning.
New evidence that post-traumatic stress syndrome is linked to an elevated risk for Alzheimer's disease was presented at an international meeting on the degenerative brain disorder this week.
But so too was evidence that some of the same destructive pathways activated in Alzheimer's are also triggered after traumatic brain injury.
At the meeting, Dr. Kristine Yaffe -- a University of California, San Francisco professor and director of the Memories Disorders Clinic at the San Francisco Veteran's Administration Medical Center -- described her study of more than 180,000 veterans 55 and older, including just over 53,000 who had been diagnosed with PTSD.
From 2001 through 2007, she and colleagues followed the almost all male vets, who had an average age just under 69, flagging those who were diagnosed with Alzheimer's or dementia.
They found that 10.6 percent of those with PTSD developed new cases of dementia over the follow-up period, compared with 6.6 percent of vets who had not been diagnosed with the stress disorder.
Even after adjusting for factors like age, race and education, as well as other medical and psychiatric conditions, PTSD patients were still nearly twice as likely to develop dementia as those without the disorder. Similar results arose even when the researchers excluded those with a history of traumatic brain injury, substance abuse or depression.
While Yaffe said more research is needed to understand the connection between the two disorders, the study makes it clear "it is critical to follow patients with PTSD and evaluate them early for dementia."
The Alzheimer's Association reports that 5.3 million Americans are living with the disorder, and that some half a million new patients are diagnosed each year. The disease is now the sixth leading cause of death in the U.S. overall, and there is no treatment to prevent, delay or reverse the degeneration, which remains difficult to diagnose, particularly at early stages.
In another presentation before the Alzheimer Association's international research conference in Vienna, scientists from Georgetown University Medical Center in Washington, D.C. showed that the same mechanisms cause the destruction of brain cells in both Alzheimer's and traumatic brain injury.
Researchers already know that people who experience traumatic brain injury are at 400-percent increased risk for developing Alzheimer's. Both disorders involve build-up of beta amyloid, a toxic brain protein.
These peptides are produced when larger brain proteins are cut by a series of enzymes inside the brain cells. Inhibiting agents that block the activity of those enzymes are already being studied as a treatment for Alzheimer's.
But the Georgetown researchers, led by neuroscientist Mark Burns, reported that giving those inhibitors to mice with brain trauma reduced the loss of neurons and protected them from motor control and cognitive deficits. Similar results have been achieved by other researchers working with genetically engineered mice that have a form of Alzheimer's.
"The goal for both diseases is to prevent neuronal cell death, and this study suggests that one therapy could possibly work for both,'' Burns said.
He noted that buildup of beta amyloid occurs in a second wave of damage to brain cells following the first loss of nerve cells to traumatic injury. This second stage of injury can go on for months, if not years, resulting in large gaps in brain tissue.
But mice treated with the experimental drug had brain injuries that were as much as 70 percent smaller than those seen in untreated animals with the same level of injury.
On the Net: http://www.alz.org
(Contact Lee Bowman at bowmanl(at)shns.com)
(Distributed by Scripps Howard News Service, http://www.scrippsnews.com)
THE MEDICAL JOURNAL
