It begins slowly and insidiously, often long before anyone is aware of it. But the end for an Alzheimer's patient is devastating. The person loses the ability to speak or to understand words, is often violent, no longer recognizes family or friends, forgets how to eat, and is totally dependent on a caregiver. 

The brain is transformed from a vibrant mass of neurons crackling with connections to a shrunken, calcified orb, filled with lesions that scientists dub plaques and tangles. 

As Canada's aging population faces an epidemic of the disease, "people are much more aware of it and prepared to talk about it," says Dr. Peter St. George-Hyslop of the University of Toronto, a geneticist internationally acclaimed for his work in the field. 

"We are now where we were with cancer 30 years ago." 

Today, World Alzheimer's Day, the focus is on new hope, but also ominous statistics. The theme organizers chose for the day is "No Time to Lose." 

About 400,000 Canadians 65 or older have Alzheimer's or a related form of dementia, and that number is projected to surpass 750,000 by 2031 - "a profound growth," says Steve Rudin, executive director of the Alzheimer Society of Canada. One in 13 Canadians 65 and up has Alzheimer's. After 85, that number jumps to one in three. 

In the past decade, remarkable progress has been made in identifying the disease, which is now known to result from the accumulation of two proteins in the brain. Brain cells shrink or disappear and are replaced by dense, irregularly shaped spots, or plaques, while thread-like tangles form within existing brain cells, choking them. 

St. George-Hyslop's team and others have identified several genes linked to the 10 to 15 per cent of people who inherit the disease. But mysteries remain. 

Four drugs have been approved that slow the disease by replacing one of the chemicals lost to Alzheimer's. "But as of right today, there really isn't anything you can do to stop the process," St. George-Hyslop says. Still, he remains hopeful. "I think most people in the field would say we know an awful lot more than we ever did before." 

Work is under way on a vaccine to block the production of the toxic beta amyloid proteins, on accelerating their removal and on preventing the protein fragments from forming into clumps or plaques. 

In 2000, St. George-Hyslop and other groups began testing a vaccine on humans after it was shown to have prevented the formation of plaques in mice. 

Six months into testing, the trial was halted because 10 per cent of patients had an allergic reaction to the vaccine, which killed two of them. 

But it had a modest positive effect on others, and that "was enough to encourage people to go back and look at what part of the vaccine is good and what part is bad," he says. 

The vaccine work "is the most exciting thing on the horizon," said Dr. Tiffany Chow, a clinical scientist at the Rotman Research Institute at the Baycrest Centre for Geriatric Care. "It's a matter of tinkering with it to make it safe." 

Drugs are also being developed to stop the protein fragments from clumping together into plaques, some of which should go into trials in the next year, says St. George-Hyslop. 

Other research is using PET scans to track the buildup of plaques and tangles, which can begin decades before they become noticeable in a patient. 

Such scans could eventually offer "early detection and treatment for people who haven't developed full-blown symptoms yet," says Dr. Paul Verhoeuf, a clinical research scientist at the Kunin-Lunenfeld Applied Research Unit at Baycrest.