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发帖数: 768 | 1 ScienceDaily (May 2, 2011) — Higher levels of cell chatter boost
amyloid beta in the brain regions that Alzheimer's hits first,
researchers at Washington University School of Medicine in St. Louis
report. Amyloid beta is the main ingredient of the plaque lesions that
are a hallmark of Alzheimer's.
These brain regions belong to a network that is more active when the
brain is at rest. The discovery that cells in these regions
communicate with each other more often than cells in other parts of
the brain may help explain why these areas are frequently among the
first to develop plaques, according to the researchers.
Working with mice genetically engineered to develop Alzheimer's
type-brain changes, scientists reduced the size and number of plaques by
decreasing brain cell activity in certain regions.
The results, appearing May 1 in Nature Neuroscience, are the latest to
hint at a resolution to lines of evidence that have suggested busier
brain cells can both contribute to and prevent Alzheimer's. According to
a new theory, which brain cells are kept busy may make all the
difference.
"Engaging the brain in tasks like reading, socializing or studying may
be helpful because they reduce activity in susceptible regions and
increase activity in regions that seem to be less vulnerable to
Alzheimer's plaque deposition," says David M. Holtzman, MD, the Andrew
B. and Gretchen P. Jones Professor and head of the Department of
Neurology. "I suspect that sleep deprivation and increased stress, which
may affect Alzheimer's risk, may also increase activity levels in these
vulnerable regions."
The susceptible regions of the brain highlighted in the new study belong
to the default mode network, a group of brain regions that become
more active when the brain is not engaged in a cognitively demanding
task. Co-author Marcus Raichle, MD, professor of neurology, of radiology
and of neurobiology, was among the first to describe the default mode
network.
In a paper published in 2005, Washington University researchers showed
that regions in the default mode network are often among the first to
develop Alzheimer's plaques. To understand why, Adam Bero, a graduate
student in Holtzman's lab, analyzed the brain chemistry of mice. He
found that the mouse brain regions analogous to those in the human
default mode network had similarly high levels of early amyloid plaque
deposits when compared to other areas.
Next, Bero showed in younger mice that the high-plaque regions had
increased amyloid beta levels. In a third experiment, he found that
the greater amyloid beta levels were caused by increased nerve cell
communication in the affected regions.
To further prove the relationship between plaque formation and cell
communication, scientists trimmed the whiskers on one side of a group of
mice and kept them short for one month.
"Because mice are nocturnal and their eyesight is poor, whiskers are
an important way for them to sense where they are in their environment,"
Holtzman explains. "By cutting the whiskers back on one side, we
reduced neuronal activity in the region of the brain that senses whisker
movement."
Loss of this input resulted in smaller and less numerous plaques on
the side of the brain connected to the pruned whiskers. In a separate
experiment, when researchers regularly stimulated whiskers with a cotton
swab, amyloid beta levels increased.
According to Holtzman, the results demonstrate the direct connection
between amyloid plaque formation and growth and changes in brain cell
activity levels in various parts of the brain. He plans further
investigations of the mechanisms that regulate default brain activity,
their connections to phenomena such as sleep, and their potential
effects on Alzheimer's disease.
Funding from the National Institutes of Health (NIH) and the Cure
Alzheimer's Fund supported this research
Journal Reference:
1.Adam W Bero, Ping Yan, Jee Hoon Roh, John R Cirrito, Floy R Stewart,
Marcus E Raichle, Jin-Moo Lee, David M Holtzman. Neuronal activity
regulates the regional vulnerability to amyloid-β deposition. Nature
Neuroscience, 2011; DOI: 10.1038/nn.2801 | h******u
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