FORT COLLINS, Colo. -- Colorado State University researchers
think insulin levels in the brain may be the key to understanding
how some types of dementia progress.
Low levels of both insulin and insulin-like growth factors
appear to cause cell loss and the shrinking of the brain that
results in dementia, the researchers found.
Douglas Ishii, a professor in the department of biomedical
sciences at Colorado State and the lead researcher in the study,
said the findings offer real hope that the progression of dementia
in people with conditions like Alzheimer's, diabetes and
Parkinson's disease may someday be prevented.
"This has been the Holy Grail in the Alzheimer's field --
halting the progression of this terrible disease," Ishii said.
The study will be published in the next issue of the journal
Brain Research. The research was funded by the National Institute
of Neurological Diseases and Stroke, Centers for Disease Control
and Prevention, and Colorado Commission on Higher Education.
Ishii, who began studying the role of insulin in brain
development more than 25 years ago, cautioned that more research --
including clinical trials -- will be required.
Likewise, the Alzheimer's Association of Colorado is heartened
by Ishii's work, but said much more research is needed before the
fight against dementia can be declared over.
"We still don't know about this disease, so much of it is still
a mystery," said Sara Spaulding, spokeswoman for the association.
More than 5 million Americans have dementia. About 10 million
baby boomers are projected to suffer Alzheimer's in their
lifetimes. By 2010, there will be nearly a half million new cases
of Alzheimer's diagnosed annually; and by 2050, there will be
nearly a million new cases per year, according to the Alzheimer's
Association.
Before the discovery by Ishii's group, researchers did not
understand what causes the brain to shrink.
That missing information made it impossible for the medical
field to develop ways to slow, stop or reverse conditions like
Alzheimer's.
Current treatments for dementia include medications that delay
the progression of symptoms while the brain continues to shrink.
"These drugs, by and large, give a little boost to learning and
memory, and they only work for a few years at best," said Ishii.
The treatments don't work for long because scientists have not
yet figured out how to cross the barrier between blood and brain
with medications. Likewise, even though a person who has
Alzheimer's or diabetes might have high levels of insulin in his
blood, the insulin in the brain may be abnormally low because of a
blockage in the blood-brain barrier, the researchers explained.
Insulin-like growth factors are proteins that support nerve cell
survival, the regeneration of nerves and the formation of synapses,
which create connections in the central nervous system.
The proteins are often low in diabetic and Alzheimer's patients,
as are insulin levels.
For many years, Ishii said, scientists have been working to
understand the link between diabetes and dementia. About 80 percent
of Alzheimer's patients have a history of diabetes or pre-diabetes.
Diabetics also are at a higher risk of developing dementia.
But previous research suggested that low insulin levels in the
brain receptors weren't related to brain shrinkage and Ishii's
earlier research found that increasing the levels of only
insulin-like growth factors does not prevent brain shrinkage.
The new study found that the gradual loss of both insulin and
insulin-like growth factors combined with aging and disease likely
increases the risk of brain shrinkage.
"For the first time," Ishii said, "it may be possible to
develop a treatment that prevents brain atrophy and prevents the
progression of dementia."