A research team has for the first time identified a
substance in the brain that is proven to cause memory loss.
This identification gives drug developers a target for
creating drugs to treat memory loss in patients with
dementia.
The team, which published its results in the March 16
issue of Nature, was led by Karen H. Ashe of the
University of Minnesota and included Michela Gallagher,
Krieger-Eisenhower Professor and chair of the
Department of
Psychological and Brain Sciences at Johns Hopkins, and
Ming T. Koh, a postdoctoral fellow in that department.
"Now that we have found a protein complex that causes
cognitive decline and loss of memory, we will be able to
aim our investigations not only to learning how that
substance is implicated in disease but also toward
prevention," Gallagher said.
More specifically, once the memory-robbing protein
complex is better understood, drugs could be developed to
stop Alzheimer's disease in its tracks, the researchers
say.
Currently about 4.5 million Americans live with
Alzheimer's disease, a number that is expected to rise to
14 million over the next two decades. In the past, it was
generally accepted that Alzheimer's disease was caused by
plaques and tangles, unnatural accumulations of two
naturally occurring proteins in the brain: amyloid-beta,
which builds into plaques between nerve cells in the brain,
and tau, which forms the tangles inside nerve cells.
Ashe's lab proved last year that the tangles are not
the cause of memory loss; this latest research shows the
plaques aren't a major cause either.
People with Alzheimer's disease exhibit memory
impairment before they are formally diagnosed, or before
nerve cells in their brains begin to die. Thus, it is often
difficult to discern whether people are experiencing the
normal memory impairment that comes with aging or if they
are, in fact, in the early stages of Alzheimer's
disease.
The researchers hypothesized that there was a
substance in the brain that causes memory decline that is
present even before nerve cells begin to die. To test that
hypothesis, the team used mice whose genetic makeup was
manipulated to develop memory loss much in the way people
develop subtle memory problems before the earliest stages
of Alzheimer's disease. Using mice that showed early signs
of memory loss and had no plaques or nerve cell loss in the
brain, they discovered a form of the amyloid-beta protein
that is distinct from plaques. They extracted and purified
this newly found protein complex and injected it into
healthy rats. The rats suffered cognitive impairment,
confirming that this protein has a detrimental effect on
memory.
Researchers at the University of Southern California
and the University of California, Irvine, also collaborated
on the research.
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