(Bloomberg) — Abnormal deposits in the brain thought to trigger Alzheimer’s disease can be detected decades before the memory-robbing illness ensues, a finding that will help guide future treatments, researchers in Australia say.
Doctors at Melbourne’s Austin Hospital followed 200 seniors, including people with Alzheimer’s disease and mild cognitive impairment, for more than three years to chart any decline in cognition and brain size against the deposition of abnormal protein in their brains. They found it takes about 20 years for the deposits, known as amyloid beta, to lead to dementia.
The findings, published this month in the medical journal the Lancet Neurology, suggests doctors have a large window of opportunity to potentially slow, or even reverse, the accumulation of amyloid beta to stave off the onset of Alzheimer’s. The disease is the main cause of dementia, which afflicts 35.6 million people globally — a number the World Health Organization says will double by 2030 and triple by 2050.
“It’s now quite clear that it’s a very slow, gradual process over a couple of decades,” says Christopher Rowe, Austin Hospital’s director of nuclear medicine. For Alzheimer’s to develop, the brain needs to accumulate large amounts of amyloid “and you need it there for a long time,” Rowe, a study co-author, says.
All Alzheimer’s disease patients have amyloid deposits in the brain, though not all people with the deposits have the disease, Rowe says.
Rowe and colleagues are now studying potential therapies to stymie amyloid plaques before they have had a chance to damage and eventually kill brain cells. If successful, the use of PET scans — which cost $1,500 to $3,500 apiece — “will explode,” Rowe said.
“You have a much greater chance of stopping a disease than trying to repair a brain that’s severely damaged,” he said. “This is the great hope now.”
Pfizer Inc., Roche Holding AG, Eli Lilly & Co., GlaxoSmithKline Plc, Elan Corp. and Prana Biotechnology Ltd. are among drugmakers racing to develop treatments for Alzheimer’s. There have been 101 unsuccessful attempts since 1998, according to the Pharmaceutical Research and Manufacturers of America. Current therapies provide some temporary symptomatic improvement.
“The problem with Alzheimer’s disease is that you don’t have an effective therapy, but we can certainly make a better diagnosis with amyloid imaging — be more precise about what’s going on with the patient and what their prognosis is — but we can’t change the course of their disease,” Rowe says.
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