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Published on: February 21, 2012
by Pamela Fayerman for The Vancouver Sun:
University of B.C. neurology research expert Dr. Pat McGeer eats ginger every day, one of his personal strategies for warding off Alzheimer’s disease. It’s something people can do to help prevent protein plaque buildup in the brain that leads to the disease, McGeer, 84, told delegates at an international science conference Monday.
Given that drug companies aren’t even close to finding an Alzheimer’s disease prevention treatment and there are no approved drugs to stop the disease progressing, McGeer said there’s evidence for people trying some safe and simple measures in their own kitchens.
Along with ginger, try blackberries, rhubarb, cinnamon, turmeric, cranberries, pomegranate and blueberries. Those foods contain enzymes that block plaque buildup, McGeer told delegates at the American Association for the Advancement of Science meeting that ended Monday in Vancouver.
Plaque is made up of beta amyloid (A-beta) protein. Studies have shown A-beta deposits, sometimes called senile plaques, are in the brain many years before memory loss and other dementia symptoms appear.
“Since the primary cause of Alzheimer’s is brain deposits of A-beta, preventing these deposits, or helping their clearance, should prevent the disease,” said McGeer, noting that he now eats the ginger because a small lab study showed ginger extract cleared A-beta aggregation in brains riddled with it.
“I’m a great believer in eating a favourable diet.”
Inflammation in the brain, like that occurring after a concussion or brain trauma, is also linked to Alzheimer’s although it is not clear if inflammation is a cause or effect of the disease. That helps explain why 15 epidemiological studies have suggested long-term use of over-the-counter anti-inflammatories like ibuprofen may reduce the risk of Alzheimer’s.
“Yet a proper, randomized clinical trial has never been done because no company wants to pay for an ibuprofen trial when it can be bought in [a store] for five cents a pill,” McGeer said.
“The cheaper the agent, the less the incentive to fund expensive clinical trials,” he said, referring to the fact that pharmaceutical companies only want to sponsor research on new drug agents they can patent and can profit from.
McGeer, who was involved in the early research on anti-inflammatories, has long contended that those who can tolerate such medication should consider using them. But he concedes that many people can’t take them because of potentially serious side-effects of gastrointestinal upset and bleeding.
McGeer, a former Olympic basketball player, said protecting the brain from trauma is also critical for Alzheimer’s prevention, as studies have demonstrated that ex-football players are 19 times more likely to get dementia.
McGeer was joined on the panel by McGill University Alzheimer’s expert Dr. Howard Chertkow; William Thies of the Chicago-based Alzheimer’s Association and genetics expert Dr. Ekaterina Rogaeva of the University of Toronto and the University of Cambridge.
Rogaeva was a late substitute for Toronto expert Dr. Peter St. George Hislop, who was called to a meeting with the prime minister of England regarding a national Alzheimer’s strategy. McGeer said it was an ironic development, since Canada’s prime minister has not made time for the same purpose, despite requests from Alzheimer’s stakeholder groups.
Rogaeva said 10 per cent of early-onset Alzheimer’s (people under age 65) can be explained by inherited genetic mutations. The vast majority (90 per cent) of cases are diagnosed in those over 65.
Although there are hundreds of genetic anomalies associated with Alzheimer’s, scientists still don’t know which are the main culprits.
Thies said even though there are now 35 million Alzheimer’s cases around the world, and numbers are expected to triple in four decades, the U.S. government investment in Alzheimer’s research is $450 million a year, compared to $6 billion on cancer, $4 billion on heart disease and $3 billion on HIV.
Chertkow, whom McGeer described as Canada’s leading Alzheimer’s clinician, said up to 20 years before a diagnosis, neuron damage is occurring in the brain, from protein misfolding, inflammation and cellular oxidation. That may be why drug trials have been disappointing; researchers are enrolling patients too late in the disease process.
He said a more promising approach may be to study cognitively normal people who have positive amyloid biomarkers or those with mild cognitive impairment.
Chertkow agreed with McGeer that some non-pharmacological interventions, such as exercise, are likely helpful. Physical activity should be in the forefront of public health recommendations since drug trials have been disappointing insofar as removing plaques from the brain, he said.
Indeed, there have been 172 drug development trial failures. “It’s hard to develop a treatment if you don’t know the cause,” he said, adding that researchers have to look beyond amyloids to inflammation and oxidative stress in the brain.
Nearly three dozen Alzheimer’s treatment or prevention trials are going on now involving non-pharmaceutical interventions like exercise, cognitive/behavioural training, transcranial magnetic stimulation and deep brain stimulation. Other trials are exploring the usefulness of immunotherapy, cholinesterase inhibitors, statins, antihypertensives, vitamin supplements, anti-diabetic medications, BACE gene mutation inhibitors, hormones, stem cell therapy, gene therapy, thalidomide, nicotine and antibiotics.
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