Alzheimer’s is the most common form of dementia and affects one in 20 Canadians over 65 — about 290,000 people. The number rises to one in four in those over 85.
Close to 75 per cent of Canadians with Alzheimer’s are women.
According to researchers at the Johns Hopkins Bloomberg School of Public Health in Baltimore, by 2050 the number of cases around the world will quadruple to around 106 million people.
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The biggest jump is projected for Asia, where 12.6 million people currently have Alzheimer’s. That’s almost half the cases in the world. By 2050, that number is expected to balloon to 62.8 million.
The researchers say a greying population worldwide will be behind the looming dementia epidemic.
But Alzheimer’s is not just a disease of the elderly. A study released by the Alzheimer Society of Canada on Jan. 5, 2009, found that 71,000 Canadians under the age of 65 are living with Alzheimer’s disease or a related dementia. Approximately 50,000 are 59 or younger.
The society predicts that within 25 years, the number of Canadians with Alzheimer’s disease or a related dementia will more than double, ranging between 1 and 1.3 million people.
The disease slowly leads to memory impairment, behavioural changes and dementia, affecting how people understand, think, remember and communicate.
There is currently no cure for Alzheimer’s, but researchers say they’ve made progress in finding out more about the disease. They believe Alzheimer’s begins to attack the brain years before the symptoms appear, so determining what causes the disease and who’s susceptible to it are critical to researchers in the field.
“We definitively know that genes are involved – familial transmission of defective genes, and also some less obvious but very interesting findings recently suggest that what we traditionally viewed as risk factors for heart disease also happen to be risk factors for Alzheimer’s,” said Dr. Judes Poirier, director of the McGill Centre for Studies in Aging, in an interview with CBC-TV in September 2006.
In January 2007, a Canadian-led research team reported finding a gene that may increase the risk of the disease. In the journal Nature Genetics, the researchers said preliminary data suggest that people with Alzheimer’s disease tend to have lower levels of SORL1 in their blood cells.
In laboratory studies, the researchers found that when they suppressed the activity of SORL1, cells made greater amounts of amyloid beta peptide, a substance that is thought to play a key role in causing Alzheimer’s.
SORL1 controls the distribution of amyloid precursor protein (APP) inside nerve cells of the brain. When working normally, SORL1 prevents APP from being degraded into A-beta, which also fosters the formation of plaques.
Researchers believe that as the amyloid accumulates, brain cells begin to die, leading to disorientation and progressive memory loss.
Possible Alzheimer’s ‘fingerprint’?
In December 2006, researchers at New York’s Weill Cornell Medical College discovered what they described as a “fingerprint” of Alzheimer’s disease. They identified a pattern of 23 proteins floating in spinal fluid that, in preliminary testing, seems to indicate Alzheimer’s with some accuracy.
Currently the only definitive way to diagnose Alzheimer’s is through autopsy. But the finding could pave the way for a test to determine whether a person may develop Alzheimer’s later in life.
Using a technology called proteomics, the researchers examined 2,000 proteins found in the spinal fluid of 34 people who died with autopsy-proven Alzheimer’s, comparing it with the spinal fluid of 34 non-demented people.
What emerged as a difference were 23 proteins, many that by themselves had never been linked to Alzheimer’s, but that together formed a fingerprint of the disease.
The researchers then looked for the same protein pattern in 28 more people. Some had symptoms of Alzheimer’s or other dementia. Others were healthy. The test indicated Alzheimer’s in nine out of 10 patients that doctors suspect have it. But it also incorrectly pointed to Alzheimer’s in three people who were healthy.
In another study — published in an Aug. 12, 2007 article in the journal Natural Medicine — scientists from the University of Rochester Medical Center in Rochester, N.Y., reported that using a protein as a “sponge” to absorb the toxic plaque that builds up in Alzheimer’s patients can halt symptoms and improve brain function.
The protein is called soluble LRP or soluble low-density lipoprotein receptor-related protein. In healthy people, it binds to and neutralizes up to 90 per cent of the amyloid beta (the toxic plaque) that is circulating in the body.
The researchers found that when they injected mice with extra LRP, the body soaked up more of the plaque and the brain also responded by reducing levels of it. The results were more dramatic in mice with symptoms of Alzheimer’s. They experienced improved learning and memory compared to mice that did not receive the extra protein. Blood flow to the brain was also improved.
The researchers are working to create a form of LRP that can be tested in people.
Diet and Alzheimer’s
Drinking fruit and vegetable juice frequently may help delay the onset of Alzheimer’s disease, a finding that reinforces the importance of a healthy diet.
Research released in August 2006 in the U.S suggests something as simple as a glass of freshly squeezed juice three or more times a week seemed to dramatically reduce the developing signs of Alzheimer’s.
As in diabetes, the disease makes the body produce more nasty oxygen radicals — damaging chemicals produced during metabolism.
Recently, researchers in California concluded Alzheimer’s is a disease of aging because part of the brain’s cleanup crew that clears away the toxic buildup of free radicals becomes less efficient, increasing susceptibility to the disease.
Our bodies use anti-oxidants in foods to neutralize the damage.
Delaying onset
To look at the effect of diet on the risk of developing Alzheimer’s, researchers in the U.S. followed almost 2,000 dementia-free people for up to 10 years, collecting information on their diet and assessing their cognitive function every two years.
They found the risk of developing signs of Alzheimer’s was 76 per cent lower among people who drank three or more servings of juice per week compared with those who drank it less than once per week.
“Fruit and vegetable juices may play an important role in delaying the onset of Alzheimer’s disease,” Dr. Qi Dai of Vanderbilt University Medical Center in Nashville, Tenn., wrote in the September 2006 issue of the American Journal of Medicine.
The researchers originally suspected anti-oxidants such as vitamin C in the juice might be protective, but clinical studies did not support the idea.
“What this new study showed is in these juices, it isn’t the vitamins that’s protective, it’s these polyphenols, and that’s the surprising thing,” Dr. Jack Diamond, scientific director of the Alzheimer’s Society of Canada, told CBC News.
Animal and cell culture studies suggest polyphenols in juice pressed from whole, fresh fruits and vegetables show a stronger neuroprotective effect than the vitamins, the team noted. Protective polyphenols are mostly found in the skin or rind of fruits and vegetables. They tend to disintegrate when heated, Diamond said.
On this side of the border, researchers have found that being bilingual all your life may reduce your chances of developing Alzheimer’s. The researchers looked at the hospital records of people who had visited the memory clinic at Baycrest Hospital in Toronto. Two-thirds had Alzheimer’s and the rest had other kinds of dementia. Half were bilingual, speaking at least two languages every day for 50 years or more.
The researchers found that for the people who spoke one language, dementia symptoms started showing up at the age of 71, on average. For bilingual people, the average age of onset of dementia symptoms was 75.
But becoming bilingual doesn’t appear to be enough to make a difference. There was little difference in the age of onset of symptoms for people who picked up a second language later in life.
Population differences
Dai’s study was part of a larger research project comparing Alzheimer’s disease and dementia in older Japanese populations living in Japan, where incidence of Alzheimer’s is low, to Japanese people living in Hawaii and Seattle, Wash. The difference in incidence rates suggests environmental factors including diet and lifestyle may be important.
Even when different populations consumed the same vitamin content, it was the people who drank more fruit and vegetable juice that gained the greatest protection.
The protective effect won’t necessarily stop Alzheimer’s, but it reduced the chances, after controlling for other factors such as smoking, education, physical activity and fat intake that could also play a role.
The benefit was enhanced in people who carried a genetic marker called apolipoprotein E that is linked to late-onset Alzheimer’s, as well as those who were not physically active.
Although the large number of people studied across populations over a long time are assets of the study, Dai cautioned it’s important for people not to jump the gun on the potential protective value of juice, and they can’t say what type of juice might help or how long it needs to be consumed.
Previously, clinical trials, a more rigorous form of research, did not pan out for using antioxidant vitamins or hormone replacement therapy to prevent or slow Alzheimer’s, Dai said.
While some dieters may be told to avoid the excess calories in juice, the research adds to evidence on how fruits and vegetables improve health. The foods help blood pressure and keep blood vessels healthy.
Canadian researchers are also looking at non-dietary strategies for curbing the nerve damage of Alzheimer’s.
Researchers at the Centre for Research in Neurodegenerative Diseases at the University of Toronto discovered a protein blocks the creation of nerve toxins in Alzheimer’s.
If scientists can understand how the protein prevents the toxic build-up, it could lead to more specific treatments with fewer side-effects, according to Dr. Georges Levesque, chair of the biomedical review panel at the Alzheimer Society of Canada.
Source: cbc.ca
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