By Paul Candon, Medical Tribune News Service
Head trauma produces damage in the brain that resembles the
injury seen in the brains of people with Alzheimer's disease,
according to researchers in Philadelphia.
``A series of studies has shown that brain trauma is the only
environmental risk factor for Alzheimer's disease,'' said Dr.
Douglas Smith, lead author of the study and associate professor of
neurosurgery in the University of Pennsylvania Medical Center.
``Patients have cognitive decline accelerated if they have a
history of brain trauma,'' he added.
For years, scientists have known that boxers can suffer from
``punch-drunk syndrome,'' characterized by tremors and a decline in
mental ability resulting from repeated head trauma. The brains of
these boxers have been found to contain abnormal tissue formations,
called tangles and plaques, which are also present in the brains of
Alzheimer's patients. Whether these abnormal tissues are the cause
or result of the disease is unknown.
To explore this link between head trauma and Alzheimer's
disease, the researchers studied a model of head trauma in pigs. In
15 anesthetized animals, they induced a form of non-impact head
injury that closely resembled the type of trauma commonly
experienced in car crashes. After comparing the brains of these
animals to those of three uninjured animals, the researchers found
accumulations of amyloid beta and tau, both hallmarks of
Alzheimer's disease. (Amyloid beta is typically found in plaques,
and tau is found in tangles.)
Specifically, these accumulations were found in the axons of the
nerve cells, extensions from the cell body that help carry chemical
messages. Further, plaque-like formations developed in a subset of
the brain-injured animals.
This is the first experimental evidence in animals to show that
Alzheimer's-like effects in the brain can be initiated by head
trauma.
Smith explained that this evidence might be of use to people who
have a genetic predisposition to the disease. Researchers in
Glasgow, Scotland, recently discovered a gene that appears to
predispose some people to Alzheimer's disease, according to Smith.
Because head trauma may increase the risk for developing
Alzheimer's and may exacerbate the symptoms in such people, ``you
might think twice about contact sports,'' he said. ``Even though
there's not a cure, there is prevention.''
Dr. Joy Snider, instructor in neurology and a researcher at the
Center for the Study of Nervous System Injury and the Memory and
Aging Project at Washington University School of Medicine, St.
Louis, said that this animal model for head injury will help in
future studies to determine how significant a factor brain trauma
is in Alzheimer's disease. ``One of the things we don't know about
Alzheimer's disease is once you get a plaque or tangle, is it there
forever, or can it be cleaned up and can it go away?'' she
remarked. Snider said that researchers can now use this model for
long-term studies to see if animals will develop Alzheimer's-like
pathology over the course of months and years.
The study appeared in the September issue of Journal of
Neuropathology and Experimental Neurology.
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Journal of Neuropathology and Experimental Neurology
(1999;58;982-992)
