Alzheimer's Cases Predicted To Rise 1000 Percent: What's Being Done To Find A Cure
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A half a million Canadians are currently stricken with Alzheimer’s, and within a generation, researchers predict that number will double to 1,100,000, according to Rising Tide, a 2010 study commissioned by the Alzheimer Society of Canada. The cost for dementia care will rise over 1000 percent from the current $15 billion to $153 billion over the same time period.
Those are some shocking numbers.
The most widespread disease of the family of “dementias,” Alzheimer’s affects 5 to 8 percent of Canadians over the age of 65 and 30 to 50 percent over 85. Once diagnosed, the patient usually dies within seven to 10 years.
Dr. Jack Diamond, scientific director, Alzheimer Society Of Canada, and author of a report on the state and current research of the malady, goes as far as to call Alzheimer’s “an epidemic,” but not by the definition of a contagion.
“It isn’t an epidemic in the sense of people catching it, but there is an epidemic in the sense of the increased numbers being newly diagnosed; the total number of people with Alzheimer’s is steadily rising worldwide,” Diamond tells www.samaritanmag.com. “First of all, we’re living longer. Age is the biggest risk factor and the longer you live, the more of a chance you have of getting it. That’s one item that’s contributing.
“Another one is earlier diagnosis. People are now taking their family members for diagnosis where previously they didn’t, so we’re getting more diagnoses. People are getting them there earlier.”
Alzheimer’s is a heartbreaking disease for the friends and family of the loved one, a progressive and eventually fatal brain disease that eradicates nerve cells and robs people of their thinking ability, memories and eventually the ability to care for themselves.
Caregivers across Canada today spend 231 million hours a year caring for someone with dementia. This number is expected to jump to 756 million hours per year within a generation.
While there have been no recent breakthroughs in treatment for Alzheimer’s disease, Diamond says research is at a “crossroads.”
“There are lots of breakthroughs claimed, but none so far have paid off,” says Diamond. “We have no effective treatment at the moment against the disease.”
While certain treatments for Alzheimer’s can show promise over one to three years, he says, “They are only symptomatic and they eventually stop working.”
“Within that timeframe, they keep symptoms at bay, which is excellent, but they’re not disease modifying. It’s as if you had a painkiller without affecting the thing that’s causing the pain. You still function well if you can keep the pain at bay. There are a lot of clinical trials going on, and we’re awaiting the results from those.”
Diamond also recites a laundry list of Alzheimer’s risk factors that, frankly, commonly lead to other afflictions: obesity, oxidative stress (toxins), high blood pressure, high cholesterol, diabetes, chronic stress and smoking.
Genetic risk factors, isolation, head trauma, strokes, clinical depression, Down’s Syndrome — and even the post-menopausal state in women — can also be contributing factors. Even low levels of formal education and low socio-economic stature have been claimed to increase one’s risk of developing Alzheimer’s.
“The risk factors include anything that’s a consequence of unhealthy living,” says Diamond, whose credentials include former positions as associate director for Scientific Affairs at the Montreal Neurological Institute at McGill University, founding Chair of the original Department of Neurosciences at McMaster University, Hamilton and Professor Emeritus in the Department of Psychiatry and Behavioural Neurosciences at McMaster.
“It isn’t inevitable, but we do know that the more likely you are to be unhealthy, the more likely you’ll get it.”
Scientists are basing their research on the findings of the disease’s namesake.
When he studied “senile dementia,” later to be renamed Alzheimer’s disease in 1906, Dr. Alois Alzheimer used a microscope and noted physical peculiarities in the brain tissue after examining, especially amyloid plaques and neurofibrillary tangles.
“These are minute things you can see under a microscope,” Diamond explains. “(Alzheimer) saw tiny deposits around the nerve cells and the plaques. Inside the nerve cells it was as if balls of wool had started to untangle — so he called them ‘the tangles.’
“He also noticed that a lot of cells had died,” Diamond continues. “So the plaques and tangles are often called hallmarks of Alzheimer’s. He really showed that this was a disease of aging and not just a consequence of aging itself.”
In recent years, however, simply using Alzheimer’s observation to quickly diagnose his disease has run into problems, Diamond says, which has led to the scientific conundrum.
“Within the last few years, [scientific] papers started appearing in which very old people — those in their 90s and 100s — died without any dementia. But their brains were full of plaques and tangles, even though they didn’t have any dementia. So there’s more to it than that.”
“So we’re now at a crossroads, going down other roads to add to what we know in order to determine what has to be present in order to cause dementia. Some of the things that we always assumed are now no longer acceptable as fully explaining the disease.”
Experiments involving mice also ran into problems.
“One of the mystifying things was that a number of drugs that were tested and worked on mice, but didn’t work on humans during clinical trials,” notes Diamond.
“So this is another hold-up: We can’t assume that something that works on mice will necessarily work on humans.”
The irrefutable research so far: According to Diamond, the pathological changes — or abnormalities — in the brain that are associated with dementia, begin decades before the dementia actually arrives.
“In other words, anybody 30 and up can have a brain in which the disease process has already started, but the dementia takes decades to appear,” says Diamond, who continues to run a laboratory research program on the apoE4 risk factor for Alzheimer’s disease. “So we have two situations: the actual changes to the brain, i.e., the pathology, and the dementia.”
Returning to the subject of amyloid plaques and tangles, Diamond says there’s a build-up around brain nerve endings that prevent the cells from communicating with one another.
“We now know that the Alzheimer’s type brain has a high level of this beta-amyloid, a normal protein that we all have, but because it accumulates in the Alzheimer’s brain as the molecules start sticking together to form plaques,” he explains.
Diamond says the usual process is that the beta-amyloid compounds is continually being made, and is continually being eliminated from, the brain.
“There’s turnover all the time,” he explains. “But when things accumulate, that’s bad news as the molecules start sticking together, forming plaque. But by the time the plaques are formed, all the damage to the nerve cells has been done. A successful treatment would have to affect the amyloid molecules, not the plaques themselves.”
Amyloid-prohibitive drugs are under clinical trials at the moment, says Diamond, including a vaccine against the amyloid protein. “Get immunized and then you sweep away the protein before it has time to do any damage,” he states.
In 2000, According to Diamond, a first batch of vaccines that successfully treated animals seemed so promising that human trials were approved. Two years later, however, two people during the trial died with inflammation of the brain. “All trials stopped,” said Diamond.
Once autopsies were performed, scientists had discovered that although the plaques had been significantly reduced, “the dementia prior to death was unchanged.”
“So if we stop the amyloid from accumulating, it doesn’t mean we’ve found the cure we need,” says Diamond.
There are a number of drugs being developed to treat Alzheimer’s: among them, the symptom-reducing ones like donepezil, rivastigmine and galantamine (“cholinesterase inhibitors” that help sick nerve endings transmit nerve messages to the next cell in the brain) and memantine hydrochloride (blocks glutamate receptors, thereby preventing the uptake and recycling of the glutamate which tends to accumulate around the sick neural cells); a variety of other drugs designed to help prevent amyloid accumulation such as vaccines; statins (cholesterol-reducing agents) and even gingko balboa and aspirin, are still in clinical trials.
Stem cell treatments are also being researched.
But on a more simple, personal level, Diamond recommends moderate exercise to help fight the disease. “A healthy lifestyle has been able to slow it down,” he says. It makes brain cells healthier and more resistant to disease, and almost certainly increases the levels of substances in the brain, which cause nerve cells to sprout new branches and make new connections. “Any activity — housework, gardening — going up and down the stairs five times a day.”
Diamond also recommends socializing and engaging in brainteasers as ways to help fight the disease. “It’s a form of environmental enrichment. Doing crosswords and things like that also help — anything which drives the brain. We know now that it’s very effective in slowing down an already present Alzheimer’s disease, and in reducing one’s chances of getting it in the first place.”THE SNEAKER BULLETIN
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