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Time
Mapping out how an Alzheimer’s gene works could lead to new treatments.
So far, nearly two dozen genes scattered across four chromosomes have been
linked to an increased risk of Alzheimer’s disease. But identifying such genetic
risk factors doesn’t mean that researchers fully understand how they contribute
to cognitive decline and dementia. And that understanding is often crucial to
turning genetic information into effective treatments.
Now a group of scientists report in the journal Neuron that they have pieced together the back story of
one gene, known as CD33, that could lead to exciting new ways of removing the
amyloid plaques that build up in the brains of Alzheimer’s patients and cause so
many problems with memory and cognitive functions.
(MORE: New Research on Understanding Alzheimer’s)
Dr. Rudolph Tanzi, director of the genetics and aging research unit at
Massachusetts General Hospital and professor of neurology at Harvard Medical
School, and his team first identified CD33 in 2008, and at the time, he says, “We had no
idea what this thing did. And in the [scientific research] literature, little
was known about it. So we started from scratch.”
Beginning with studies of the where the gene was expressed, he found that a
subset of brain cells known as microglia seemed to show high levels of CD33,
which makes receptors that pop up on the surface of the cells to bind to
neuronal debris, including the residue of inflammatory reactions, and dead and
dying nerve cells. CD33 functions as a molecular housekeeper, patrolling the
nervous system for any material that doesn’t belong and could impair normal
brain function. That includes the deposits of amyloid protein that build up in
the brains of Alzheimer’s patients, eventually forming sticky plaques that
compromise normal nerve function before destroying them.
(MORE: First Genes Linked to Higher Risk of Alzheimer’s Disease Among
African-Americans)
But when Tanzi’s team looked at the brains of patients who had died of
Alzheimer’s, they found that CD33 also had a darker side. In patients with a
higher burden of amyloid plaques, CD33 also appeared in excess. And so did tons
of dead neurons. “At some point, as the amyloid is making the cells sick, and
forming tangles as lots of neurons are dying, the microglia put on their battle
gear and turn radical, killing whatever they think is attacking the brain,” says
Tanzi. “The result is friendly fire, and they start to kill so many neurons that
the microglia are now detrimental; they are no longer clearing but they’re
rounding up nerve cells and shooting out free radicals and causing a lot of
damage.”
Instead of engulfing and removing the amyloid, microglia armed with CD33 were
targeting healthy nerves instead. To confirm that, Tanzi’s team conducted a
series of tests with cells in culture and in animals, and found that when
microglia were stripped of CD33, they went back to performing their housekeeping
duties as expected, sniffing out amyloid and pulling the protein out of
circulation. Mice genetically engineered to develop Alzheimer’s plaques but
without CD33 showed lower levels of amyloid plaques in their brains than animals
with the gene, suggesting that the CD33 was clearing the protein away.
(MORE: Genetic Markers May Predict Increased Risk of Alzheimer’s)
That clearance could be the key to alleviating some of the worst symptoms of
the disease, experts say, since most people make amyloid protein but for some
reason it starts to accumulate as we age. “What we discovered is that CD33 is a
key switch so when the switch is off, and it is deactivated, there is more
clearance of [amyloid,]” says Tanzi. “If we can now find drugs that inactivate
CD33 it should allow more clearance of [amyloid] by the microglial cells.”
His group is already screening compounds to find those that might block CD33
from turning rogue, but the search will have to balance compounds that do a good
job of keeping CD33 honest without compromising its ability to seek and destroy
real invaders, as it was designed to do. “It’s something we have to keep an eye
on for sure,” says Tanzi of the possibility that a CD33 blocker to treat
Alzheimer’s could compromise immune functions and make patients more vulnerable
to infections or other health issues.
But the discovery could be an important step toward finally developing an
effective Alzheimer’s drug treatment, since clearing amyloid plaques could be
critical in addressing the deposits of amyloid that mushroom throughout the
brain as the disease progresses. “We just need to take advantage of the
housekeeping functions of CD33 and entice them to stay helpful and not go
crazy,” says Tanzi.
MORE: Two Studies Find Promising New Ways to Detect Alzheimer’s
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