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Alzheimer’s Stopped in Modified Mice Brains that
Also Allow for More Study
Nov. 16, 2005 – Scientist report they have
developed a new strain of genetically modified mice that allow them to
stop the development of Alzheimer’s disease and to work on potential new
therapies for the disease.
This discovery has helped scientists evaluate the
brain's ability to repair one of Alzheimer's hallmark lesions, senile
plaque.
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More news on Alzheimer's Disease &
Dementia - click here. |
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These plaques occur when enzymes - proteins that
cause or speed up chemical reactions - create peptide fragments called
beta amyloid, also known as Abeta. The fragments clump together to form
senile plaques, clogging the spaces between cells and damaging parts of
the brain used for memory and decision-making.
The mice were genetically engineered by scientists
to respond to a type of therapy designed to lower production of Abeta by
inhibiting the enzymes responsible for peptide release.
"We can stop the disease from getting worse in
these mice, but we can't reverse it," said David Borchelt, Ph.D., a
professor of neuroscience at the McKnight Brain Institute of the
University of Florida. "Although it is possible that human brains repair
damage better than mouse brains, the study suggests that it may be
difficult to repair lesions once they've formed."
The development by researchers with the University
of Florida and the California Institute of Technology was reported
yesterday in the international open-access medical journal PloS
Medicine.
The need to recognize and treat Alzheimer's
patients at the first signs of impairment will be important to the
success of potential treatments, said Joanna Jankowsky, Ph.D., a
biologist at the California Institute of Technology and first author of
the paper.
"The popular expectation was once the peptide
accumulating into the plaques went away, the plaque itself would
dissolve," Jankowsky said. "But it may be similar to coronary artery
disease - once plaques start to occlude your arteries, it's not clear
that stopping the contribution to growth will make the occlusion break
up and go away."
Alzheimer's disease is a form of dementia, a brain
disorder that trips up the thoughts, memory and language skills of about
4.5 million Americans. It is not a normal outcome of aging, but the
disease affects about 5 percent of men and women ages 65 to 74,
according to the National Institute on Aging. Nearly half of people 85
and older may have it.
Drugs collectively known as secretase inhibitors
are currently in development and are based on the theory that lowering
production of Abeta could halt progression of disease and perhaps
reverse symptoms.
In the first experiments to test the idea in a
mouse model, scientists engineered 25 mice to carry two artificial
genes, one designed to continuously produce Abeta in their brains and
the other to turn off Abeta production. The "off switch" was triggered
when the antibiotic tetracycline was added to the animals' food.
With Abeta production in full swing, the brains of
mice at 6 months of age were filled with plaques. When the researchers
switched the system off, they found the existing plaques did not grow or
spread, but they did not go away, either.
"Early treatment will be important to prevent
plaque from forming," said Borchelt. "It's likely enzyme inhibitors will
work best at the first sign of mild cognitive impairment, when people
are first starting to have memory problems in early stages of
Alzheimer's disease."
Scientists from the Johns Hopkins School of
Medicine, the Mayo Clinic Jacksonville and the National Cancer Institute
made major contributions to the research, Borchelt said.
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