ful marinade it brings, might be a central
cause of the disease. Other studies are
turning up links between Alzheimer’s and
the curious tendency of brain cells under
stress to double their genetic material.
While the cause of Alzheimer’s
remains elusive, the extent of its threat
to the brain is becoming increasingly
clear. Each week, new studies chronicle
the damage in ever more detail: Chemicals that carry messages between nerve
cells go MIA, brain cells’ birthrates
plummet, cells’ energy output goes haywire, cell waste begins to pile up and
harmful reactive chemicals get produced. Ultimately, brain cells die.
Teasing apart this tangled web —in
which it’s nearly impossible to distinguish a diabolical mastermind from a
lowly hired gun or even an innocent
bystander —isn’t easy. If it were, the
problem would be solved by now. “I
think we have to be honest and say this
is an incredibly complicated condition,
and it’s going to be very hard to tackle
it,” says Alzheimer’s researcher Lennart
Mucke of the University of California,
San Francisco.
Alzheimer’s boom as the baby boomers age, the number of
elderly americans with alzheimer’s is projected to reach 13. 5 million by 2050. assuming no breakthroughs in treatment, health care
costs will continue to increase as well.
Projected Americans age 65 and over with Alzheimer’s
14
13. 5
12. 7
Number of Americans in millions
12
11. 2
10
9. 5
8
7. 8
6. 5
6
5. 1 5. 3 5. 6
4
2
0
In the tangle of
Alzheimer’s, one thing
is clear: Old age is
the No. 1 risk factor, a
frightening realization
as the front edge of
the baby boomer tide
turns 65 this year. The
disease is “obviously an
epidemic of staggering
proportions, and obviously of great economic
impact,” says neuroscientist Sam Sisodia
of the University of
Chicago. Alzheimer’s
is the fastest growing
cause of death from major disorders in
the United States, and a recent analysis
estimates that the nation’s annual cost
of Alzheimer’s-related care will exceed
$1 trillion by 2050.
Alzheimer’s is unlike anything else
clinicians have treated: In most cases,
no one knows what causes it. It can’t be
definitively diagnosed until a patholo-gist cuts into the dead brain. There is
no known cure or therapy for prevention, and even if there were, it wouldn’t
be clear when to use either one. Many
believe the disease causes its irreparable
damage years before symptoms appear.
“We have therapies that help with the
symptoms, but we don’t have disease-
modifying treatments,” says Paul Aisen
of the University of California, San Diego
School of Medicine, a neurologist who
tests potential Alzheimer’s drugs. “And
we don’t know what the best target is, and
we don’t know what the best timing is.”
But many scientists in the field find
hope in the fact that they have sketched
out the broad outline of how the disease
works, pointing to new targets for ther-
apies. One key to filling in that sketch,
scientists now know, is understanding
brain cell communication.
2010 2015 2020 2025 2030 2035 2040 2050 2045
Year
source: alzheimer’s association
A tangled web
It’s no surprise that A-beta has attracted
so much attention from those intent on
unraveling the mysteries of Alzheimer’s.
Ominous deposits of the protein (along
with tangles of another protein, called
tau, that has also garnered a fair share of
investigation) were what caught the eye
of German physician Alois Alzheimer
when he first described the disease a little over a century ago. His postmortem
exam of a patient’s brain revealed the
amyloid plaques that have been associated with Alzheimer’s disease ever since.
But much remains unknown about
A-beta. While it has been shown that
A-beta is a snippet cut from the larger
amyloid precursor protein, found in
nearly every cell in perfectly healthy
brains, A-beta’s normal function remains
murky. Studies have hinted that the protein might aid nerve cell activity or combat dangerous pathogens. Others suggest
A-beta is merely a cellular by-product
that adopted a new and damaging role.
Brain chatter, interrupted
A-beta scrambles neural dispatches
in an unexpected way, new work from
neuroscientist Gabriel Silva of the Uni-
versity of California, San Diego suggests.
In a dish of brain cells called astrocytes,
a droplet of the A-beta protein sparked a
signal that can silence chatter between
nerve cells, the brain’s main communi-
cators. The signal traveled as a wave of
calcium atoms that washed across cells,
kicking off a series of damaging events
that could end with disrupted nerve cell
communication.
www.sciencenews.org
march 12, 2011 | science news | 25
