"The dilemma is, can you treat people as if they have Alzheimer's if they do not?" said Koo, co-director of the Shiley-Marcos Alzheimer's Disease Research Center at UC San Diego. "That's the catch-22."
Most proposed Alzheimer's disease therapies target so-called "brain plaques" proteins that clog the spaces between brain cells. Experimental models suggest that therapies targeting these proteins, known as amyloid beta-peptide, may be effective.
Approximately 90 experimental therapies intended to slow or stop the progression of the disease are under way, many of them targeting Alzheimer's hallmark brain plaques, according to the Alzheimer's Association. The problem is the strategies are likely to be much less effective when tested in patients who are already experiencing confusion, memory loss or personality changes.
But simply placing more emphasis on prevention has its own complications, the researchers say. To date, no drug candidates have been found to be effective at prevention or suitably safe enough for a patient to take for a lifetime.
And even if such a drug were found, clinical testing would take well more than a decade and cost pharmaceutical companies millions of dollars. If the drug were successful and there is no guarantee the company's patent would expire before it had a chance to recover its expenses.
"It is important to find ways to ensure that the commercial sector will invest in prevention trials that may take 10 years or more to complete," Koo said.
The authors said they are not the first to point out misalignment between clinical and preclinical studies, or summarize current therapeutics, or critique how trials are conducted.
But by presenting
|Contact: John Pastor|
University of Florida