Alzheimer's Discovery Could Curb Spread of Disease,
Researchers Say

Niamh Scallan, 
Toronto Star Staff Reporter
February 3, 2012
http://www.thestar.com/living/article/1125594--alzheimer-s-discovery-could-curb-spread-of-disease-researchers-say

Alzheimer's disease appears to spread like a virus from
one brain cell to another, a groundbreaking discovery
that could help stop the debilitating disease in its
tracks, researchers say.

Two independent studies by teams of Columbia and Harvard
researchers looked at the brains of mice and found that
the degenerative brain disease begins in one small part
of the brain and spreads through an abnormal protein
known as tau, which is seen in Alzheimer's-affected
brains.

It's long been known that dying, tau-filled cells are an
early sign of Alzheimer's disease. They first appear in
the entorhinal cortex, a small area of the brain behind
the ears that controls memory and navigation and form
tangles. The disease then spreads to other areas of the
brain.

But exactly how the disease spreads remained a decades-
old enigma.

Some researchers pointed to the "bad neighbourhoods"
analogy - that Alzheimer's spontaneously appears in
vulnerable parts of the brain. Others argued that the
disease begins in one area of the brain and spreads
through a connected path to other regions that control
memory and reason.

The latest discovery, proving the latter, may now offer
scientists a way to move forward and develop a way to
block tau's spread in Alzheimer's patients, said Karen
Duff, a researcher at Columbia's Taub Institute for
Research on Alzheimer's disease and co-author of one
study published Wednesday in journal PLoS One.

"It's enlightening for us because it now provides a
whole other area for potential therapeutic impact," said
Duff. "It's possible that you can identify the disease
and intervene (with potential tau-blocking drugs) before
the dementia actually sets in."

The findings come as countries worldwide grapple with
rising rates of the debilitating disease. Roughly
500,000 Canadians are living with Alzheimer's or other
forms of dementia, according to the Alzheimer Society of
Canada. By 2028, that number is expected to rise to 1.1
million at an annual cost of $153 billion.

In the Columbia study, researchers began three years ago
examining the brains of people who died from the
disease. From that research, they genetically engineered
mice so that each rodent could produce abnormal tau
proteins. In doing this, the mice brains mimicked those
of patients in Alzheimer's early stages.

In healthy people, tau protein acts as a sort of
supportive scaffolding inside the nerve cell. But in
Alzheimer's patients, the tau protein distorts and loses
its ability to hold the cell together. It clumps
together into a messy tangle and spreads like a virus
throughout brain, destroying cells and affecting memory
and reason.

Over a two-year period, researchers examined the mice
and found that the dying, tau-filled cells in the
entorhinal cortex spread outward, jumping from one cell
to another in a connected network and destroying once-
healthy nerve cells along the way.

"We were surprised," said Duff. "The idea that tau can
actually leave one cell and go into another is really,
fairly radical."

In the Harvard study, co-authored by Dr. Bradley Hyman,
director of the Alzheimer's disease Research Center at
Massachusetts General Hospital and slated for publishing
in journal Neuron in late February, researchers found
very similar results.

"This gives us the tools that we're going to need in
order to go forward and really try to help our
patients," said Hyman. "And if that's the case, it would
be very exciting."

Dr. Gerold Schmitt-Ulms, an associate professor with the
University of Toronto's Centre for Research in
Neurodegenerative Diseases, called the findings "a major
advance" in Alzheimer's research. He also said the
methods could prove important in further research into
the debilitating disease.

Though the studies break new ground in Alzheimer's
research, Schmitt-Ulms said "there's more work to be
done."

He pointed to the need to better understand the
mechanisms of other Alzheimer's-related pathogens,
including beta-amyloid, fragments of protein secreted
from nerve cells that clump together and form a
debilitating plaque between cells in the brain.

Duff said she and her team at Columbia University plan
to push forward with their research to find a way to
further verify their discovery - and find a way to block
the spread of tau and prevent people with early
Alzheimer's symptoms from further decline.

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