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Alzheimer's, Dementia, Mental Health
A Sweet Solution to Alzheimer's Disease?
Sugar restored
cognitive ability, returned mice to live normal lives
June 13, 2006 - Certain variants of a simple sugar cause
improvement in Alzheimer's-like disease in mice, according to a new
study by Canadian researchers. Although the new studies are still in
the early stages, the findings could lead to new therapies that
prevent or delay the onset of Alzheimer's disease.
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The new studies show that some types of a sugar
called cyclohexanehexol—also known as inositol—prevented the
accumulation of amyloid B deposits, a hallmark of Alzheimer's
disease.
Scyllo-inositol treatment also improved cognitive abilities
in the mice and allowed them to live a normal lifetime. The study
appeared in advance online publication of the journal Nature
Medicine on June 11, 2006.
HHMI international research scholar and senior
author Peter St George-Hyslop cautioned that the chemicals tested in
these studies are not the type of inositol sold commercially as a
nutritional supplement. That type—myo-inositol—has been shown
previously to be ineffective at breaking up amyloid aggregates, he
said.
In the brain of a person with Alzheimer's
disease, small proteins called amyloid B aggregate into plaques, and
a protein called tau clumps into neurofibrillary tangles. The brain
becomes inflamed and neurons atrophy and die.
It's not completely
clear what kind of amyloid B peptide (monomers, oligomeric
aggregates, or fibrillar aggregates) is responsible for the onset of
disease, said St George-Hyslop of the University of Toronto.
"Because we were able to show that scyllo-inositol specifically
dispersed the high-molecular-weight oligomeric aggregates, this
study confirms that the initiating event is the accumulation of
oligomeric aggregates of amyloid B peptide,” he said.
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“Alzheimer's disease is probably going to be treated by
a cocktail of drugs.”
Peter St George-Hyslop |
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Previous work by JoAnne McLaurin, also of the
University of Toronto and lead author of the Nature Medicine paper,
showed that several types of inositol could stop amyloid proteins
from aggregating in test tubes. To see if these compounds could do
the same in vivo, St George-Hyslop, McLaurin, and colleagues tested
them in transgenic mice with human genes that predispose them to an
Alzheimer's-like disease.
When the researchers treated these mice with
scyllo-inositol, all of the animals' disease symptoms improved.
Cognitive function was improved, amyloid plaques disappeared,
inflammation declined, and the mice lived longer.
The scientists found that scyllo-inositol
conferred these benefits not only if the mice were treated when they
were very young and disease-free, but also if they were treated
after the onset of disease.
As a model system, these mice “are pretty good,
but they're not a perfect replica of the disease,” St George-Hyslop
said. The mice do not develop tau tangles, he explained, but they
are prone to amyloid plaques, brain inflammation, cognitive
disturbance, and early death, just like humans with Alzheimer's
disease.
The researchers found that scyllo-inositol
worked better than the epi-inositol version. Scyllo-inositol
produced more dramatic benefits overall, while epi-inositol worked
only transiently and only when given before disease symptoms
appeared.
Scyllo-inositol “is an exciting experimental
therapy, but until it has actually been tested in humans, it should
not be considered the cure for Alzheimer's disease,” St George-Hyslop
said. “There are many things that are very promising when done in
animal models that turn out to either not work in humans or to have
unexpected toxicity.”
A public Canadian company called Transition
Therapeutics has regulatory approval for clinical trials of
scyllo-inositol in humans with Alzheimer's disease. Phase one trials
began about a week ago. St George-Hyslop has a small financial
interest in the company.
St George-Hyslop and his colleagues are
optimistic that scyllo-inositol will be less toxic to humans than
some previous drug candidates for Alzheimer's disease. A vaccine
designed to destroy amyloid B, for example, was first tested
successfully in the same type of mice used in the scyllo-inositol
studies, but the vaccine turned out to be toxic in some humans. It
caused an autoimmune reaction in about 10 percent of patients who
were immunized, St George-Hyslop said.
Autoimmune responses shouldn't be a problem
with scyllo-inositol. “This compound works by a different mechanism
and doesn't involve immunizing a patient with his own protein, which
was probably the origin of the allergic reaction to the vaccine,"
the researcher said.
Another complication with previous attempts to
treat Alzheimer's disease has been that some compounds—such as beta
secretase inhibitors—cannot enter the brain easily, St George-Hyslop
explained. Scyllo-inositol, on the other hand, readily passes
through the blood-brain barrier where it is made available to the
central nervous system.
Even if scyllo-inositol does prove safe and
effective in humans, patients will likely still need drugs designed
to attack other aspects of Alzheimer's pathology, such as tau
neurofibrillary tangles, St George-Hyslop said.
“Alzheimer's disease is probably going to be
treated by a cocktail of drugs,” he predicted. “Some of them might
be this compound, or one like it, that blocks the toxicity and
aggregation of amyloid.”
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