Stress Takes Toll on Brain
By LAURAN NEERGAARD
Associated Press Medical Writer
January 18, 2002
WASHINGTON (AP) —
Short bouts of stress caused the brain cells of mice to become
hypersensitive for weeks, says a new report seeking to uncover the
molecular root of post-traumatic stress disorder.
It's not clear if human
brain cells react the same way. But the research, by Israeli scientists,
is generating interest among scientists struggling to unravel traumatic
stress in the aftermath of terrorism.
``It's a tantalizing
new lead,'' said Rockefeller University professor Bruce McEwen, who
researches stress effects on the brain.
Anyone who has ever
experienced trauma knows such experiences can leave you nervous, easily
startled. It's one way the body protects itself from future harm, by
learning from a bad experience. But in some people, this protective
mechanism goes too far, leading to high anxiety, nightmares and
flashbacks known as post-traumatic stress disorder.
No one knows just what
happens to switch a normal stress response to an abnormal, hyper
But in Friday's edition
of the journal Science, Hermona Soreq and colleagues at Hebrew
University argue a key player is a brain protein called
acetylcholinesterase, or AChE, that is important in helping messages
jump from one neuron to the next.
Soreq exposed mouse
brain cells to AChE-affecting chemicals, including the stress hormone
cortisol, and examined the brain tissue of mice stressed in such ways as
forcing them to swim.
relatively short periods of stress caused the mice to produce a usually
rare, abnormal version of AChE that doesn't provide the same help in
That somehow left the
mice's neurons hypersensitive. Brain scans found higher levels of
electrical activity that lasted for weeks, a lengthy effect Soreq called
Soreq also works for an
Israeli drug company attempting to create an AChE-targeting treatment
for traumatic stress. One of the mouse cell studies suggested a chemical
called EN101 could be a candidate for further study.
Sometimes, ``we need
stress responses. ... We need to be more alert, we need neurons to be
active when the situation calls for that,'' Soreq said. But, ``our
findings show that traumatic experiences as well as certain chemicals do
have long-lasting effects, and that repeated stress may cause cumulative
similarities in symptoms between patients with post-traumatic stress
disorder and people poisoned by agricultural chemicals that target the
cholinergic system. That system is involved in how the brain stays
vigilant. AChE interactions with other brain chemicals have also been
associated with memory and behavior.
But it's far from the
only theory behind post-traumatic stress disorder, cautioned
Rockefeller's McEwen. On Jan. 29, he is hosting a special lecture in New
York City for people worried about the effects of the Sept. 11 terrorist
attack, where scientists from five universities will put into laymen's
terms all that is known about stressing the brain.
Based on a study that
blocking certain cell receptors inhibits the formation of bad memories,
some researchers are exploring whether beta-blocking drugs might prove
stress-protective, McEwen said.
Other research shows
the actual brain circuitry in a region called the amygdala changes after
an animal is stressed, findings generating intense interest.
Even newer studies
suggest trauma victims whose bodies produced less of the stress-related
hormone cortisol in the aftermath were more likely to develop
post-traumatic stress disorder.
The disorder ``is a
very complicated phenomenon in which various hormones in the body and
various systems in the brain may all be involved,'' McEwen notes. While
Soreq's abnormal AChE may indeed play a role, ``it's far from clear
exactly how and where.'
But regardless of what
causes post-traumatic stress, the good news is ``the brain is very
resilient. Many of these changes are not irreversible,'' he said.