New Tests, Treatments Close in on Alzheimer's
Earlier diagnosis and targeted therapies are coming, researchers say
TUESDAY, June 12, 2007 (HealthDay News) -- Doctors may soon have new tests to detect Alzheimer's early on, as well as better medications to help treat the mind-wasting disease, researchers say.
A number of advances against the disease were highlighted Monday at the Alzheimer's Association's International Conference on Prevention of Dementia in Washington, D.C.
In one presentation, researchers reported that a new test may spot Alzheimer's early. And as effective therapies become available, earlier diagnosis will be key, experts say.
"Alzheimer's disease is very difficult to diagnose when it is in its early stages," said lead researcher Geert De Meyer, a senior biostatistician at Innogenetics in Gent, Belgium. "That's a pity because therapy might be most effective when it is applied in an early stage."
In the study, De Meyer's team tested a new diagnostic test, called INNO-BIA, that detects and measures the amount of various forms of amyloid-beta protein in blood. A buildup of amyloid-beta in the brain is a hallmark, and possible cause, of Alzheimer's.
The Belgian group tried the early detection test on blood samples taken from 556 people who had come to memory clinics with the early symptoms of dementia, including mild cognitive impairment.
According to the researchers, people at risk for Alzheimer's had significantly different amyloid-beta levels in their blood compared with people who did not show risk of Alzheimer's. For example, the ratio of amyloid-beta 1-42/amyloid-beta 40 was decreased by about 20 percent in patients at risk for Alzheimer's, compared to those not at risk.
"This is really a first step," De Meyer said. "The test could be used as a screening test or a risk-factor-determining test for Alzheimer's disease that can be followed up with other tests."
Another report focused on a phase II trial that tested LY450139, a drug being developed by Eli Lilly and Company. The medication is a potential treatment for Alzheimer's because it inhibits an enzyme, known as gamma-secretase, which contributes to the formation of amyloid-beta.
The trial was led by Dr. Eric Siemers, medical director of the Eli Lilly Alzheimer's Disease Team in Indianapolis. Siemers and his colleagues randomly assigned 51 patients with mild to moderate Alzheimer's to either 100 milligrams or 140 milligrams of the drug for six to 12 weeks.
The result: Levels of amyloid-beta 1-40 were reduced by 58 percent for the 100 milligram group and by 64 percent for the 140 milligram group.
However, no differences were seen in patients' cognitive function. But Siemers isnt disheartened by that outcome, he said, since "this was too short of a period to see a disease-modifying effect."
"This is the most robust effect of amyloid-beta in blood of any drug that is currently under development," he added. "The drug was safe, but we found some things that we will continue to monitor as we go into phase III studies, which will start early next year."
A third study presented Monday tackled Alzheimer's disease from a whole different angle. Experts know that glucose is the primary energy source for brain cells. However, in people with Alzheimer's, scientists have now discovered that a dramatic dip in glucose use in certain brain areas starts 10 to 20 years before any symptoms of Alzheimer's appear.
Deprived of their primary energy source, these stricken neurons suffer irreparable damage.
"This is a very novel approach to the treatment of Alzheimer's disease," said lead researcher Lauren Costantini, vice president for clinical development at Accera, in Broomfield, Colo. "The problem that we are focusing on is reduced brain glucose metabolism that has been shown to be an early event in Alzheimer's disease."
To replace this loss, scientists at Accera have developed a milkshake-like drug called AC-1202 (Ketasyn) that provides glucose-deprived neurons with an alternative energy source, known as ketone bodies. The researchers believe that increasing the availability of ketone bodies will improve memory problems and other functional losses that occur with Alzheimer's.
Costantini's team found that, after 45 days, people who took AC-1202 had statistically significant improvement in cognition compared with people taking a placebo. The best response was seen among people who did not have the E4 variant of the apolipoprotein gene (ApoE4), which occurs in half of all Alzheimer's patients.
Those who continued to take the drug for nine months had very little disease progression, especially among the people without the E4 variant, Costantini reported.
"We see this as a potential co-therapy with other strategies," Costantini said.
For more information on Alzheimer's, visit the Alzheimer's Association.