Fantastic 4

Volume 5, Number 1
By Victoria Leenders-Cheng

Over the past decade, McGill has used the federal Canada Research Chairs program to recruit exceptional researchers from around the world. Now meet the University’s four newest CRCs.

Professor Antoine Bechara

Antoine Bechara


The holder of North America’s only joint appointment in Psychiatry and Management, Antoine Bechara divides his research on the neurology of decision-making into two camps: addiction and preventive health.

“Neuroscience tells us that food is no different than drugs or alcohol,” says the California transplant, who arrived at McGill in September 2009. “It’s addictive. As with alcohol or narcotics, high-calorie food has the potential for triggering dopamine release and that’s why people prefer it.”

Bechara is studying the neural systems, genes and behavioural mechanisms that underlie food choices and habits—insights that may, he says, help us “fool the brain into making better decisions.” Given, for example, that reward systems in the brain also trigger dopamine release, could a particular kind of non-food incentive entice an individual to choose a small meal over a larger one? Maybe. Fast food chains regularly use this reward technique, Bechara points out, as when they offer scratch-and- win cards as incentives for customers to upsize their meals, or include toys in combos marketed to children. Using fMRI scans of individuals making decisions, and studies comparing the behavior of overweight and low-weight subjects, Bechara hopes to explain the neural effect of incentives and food choices.

Bechara’s work also includes studies on how patients with focal brain lesions experience changed eating behaviours. He hopes to apply this knowledge about human neurology directly to economics as part of the Desautels Faculty of Management’s “Brain-to-Society” agenda. “This is what I call translational marketing,” he says. “We’re translating something about basic brain science into marketing and into the business world.”

Medical research and profit-driven business models often work in opposition to each other, he adds. “Medicine always says fast food is bad because they’re making all those unhealthy foods. But the food industry isn’t out to intentionally harm people—they’re selling what people like. I’m approaching this conflict scientifically, creating a new research perspective that understands the problem a little bit better to find a happy medium between the two.”

Professor John Dalton

John Dalton


The sprawling greenery of the Macdonald campus, visible from John Dalton’s office at the Institute of Parasitology, provides a vivid contrast to the minute scale of the organisms of tropical and animal infectious diseases he studies in the laboratory.

Dalton leads a team of scientists investigating how par a sites use enzymes called proteases to break down proteins in their human hosts. The cellular parasite malaria, for example, uses proteases to break down the hemoglobin in red blood cells, stealing the resulting amino acids to use as building blocks for its own growth. Malaria is endemic throughout most of Africa, Southeast Asia and Latin America, causing an estimated 300 to 500 million clinical cases and 1 to 3 million deaths annually.

By identifying the enzymes parasites use to pillage host cells, Dalton says, scientists can design drugs to prevent the parasite from growing. In 2009, his team showed that protease inhibitors kill the malaria parasite inside the cell, paving the way for the development of a new class of urgently needed anti-malarials. His team is currently preparing to test specific enzyme inhibitors using malaria grown in incubators; animal and human trials will follow in the next few years.

With worms, which are tissue-level parasites, protease research has even further-reaching implications. In studying parasites’ protease effects on their hosts, Dalton found that many worms release these enzymes not only for feeding activity but also as a way of manipulating the host’s immune response in their favour, switching off key cellular signals between the white blood cells and the T-helper cells. A compromised immune system is less protective of the body, allowing the worm to survive and reproduce for years. Understanding this mechanism could change not only our understanding of parasites affecting billions of people, but also of common immune-related diseases such as arthritis, multiple sclerosis and Type 1 diabetes.

“These are all diseases where the immune system turns on the body and damages your own tissues,” he says. “If we can figure out how worms control the immune system, we might be able to use that information to treat systems that have gone wrong for other reasons.”

Professor Jay Kaufman

Jay Kaufman


Questions about human identity and health disparity lie at the heart of social epidemiologist Jay Kaufman’s work. Why do some populations experience higher rates of chronic or infectious diseases than others? And what does it say about us as a society if these disparities correspond to differences in race, ethnicity, gender or sexual orientation?

In Canada, for example, existing studies of newborn children among indigenous populations show a much higher risk of adverse birth outcomes such as pre-term delivery or low birth weight. In Chile, however, where Kaufman has conducted preliminary comparative research, indigenous women shared the same socio-economic disadvantages as their Canadian counterparts, yet were at no higher risk for adverse birth outcomes than other Chilean women. His ongoing studies are exploring nutritional, psychosocial and health services factors to understand how the indigenous women in Chile do so well during pregnancy despite their higher risk profile.

“I’m interested in finding out more about comparisons in terms of social structure and how people live, their social opportunities, issues of discrimination, medical care,” he says, “as well as how health care systems are organized in these countries and how that manifests itself in these kinds of disparities.”

Kaufman is also very interested in how quantitative methodology can reflect existing ideologies rather than data. He cites 19th-century physician Samuel Morton, who attempted to measure intelligence by counting how many lead pellets he could fit in skulls of people of European and of African origin. (The idea may seem laughable now, but it was considered highly scientific at the time.) “The skulls were not really different in size but Morton always managed to squeeze a few extra BBs into the skulls of the whites. Our modern statistical techniques often allow for similarly unconscious fudging to confirm our existing beliefs or strong social expectations, which is why the careful study of methodology is especially important.”

To prevent such improprieties in the future, Kaufman is working toward establishing a “thoughtfully quantitative foundation” for social epidemiology. “Should disparities be measured on the absolute scale or the relative scale?” he wonders. “The prevailing ideology in biomedical research is to see demographic categories like race and gender first and foremost as intrinsic, which often translates into ‘genetic.’ But this view is narrow and worrisome, since race, ethnicity and gender mean very different things in different settings.

“Health disparities are among the most profound inequalities that threaten any society, and yet they can’t be understood merely in terms of biological traits. I’m looking at fundamental questions about issues of technology and methodology and science on one side—and about our identity, our sense of ourselves, on the other.”

Professor Alan Spatz

Alan Spatz


Like pieces of a large and complex puzzle, the different branches of pathologist Dr. Alan Spatz’s research have slowly come together to offer a clearer picture of critical cancer pathways, pointing to new cancer treatment possibilities.

Dr. Spatz comes to McGill from the Gustave-Roussy Institute in Villejuif, France. His prior research demonstrated that hereditary genetics, based on the differing make-up of the sex chromosome in females (XX) and in males (XY), means that the same cancer progresses differently in women than in men.

“We’ve known since [British geneticist] Mary Lyon’s work half a century ago that in females, one of the X chromosomes has to be silenced to keep a functional dosage of different genes, to avoid having genes in double dose,” he explains.

Building on this model, Dr. Spatz conducted in vivo studies of cutaneous melanoma, the most lethal form of skin cancer. He found that if a certain gene defect occurs on the active X chromosome, it leads to a cancer or tumour. If the same defect occurs on the silenced X chromosome, however, disease is unlikely.

These results point to the role of skewed X chromosome inactivation in cancer progression. “We now have data about the role of the X chromosome inactivation machinery in the silencing of autosomal genes,” says Dr. Spatz. “I’m totally convinced that this could lead to the identification of totally new biological processes in cancer development.”

Dr. Spatz’s work on gene silencing also led him to identify a particular gene as a fruitful target for further research. “PPP2R3B,” as it’s known, is found on the Y chromosome in males and on the X chromo some in females— and it es capes silencing on the inactive female X. Its loss or inactivation is associated with short survival in melanomas. Importantly, PPP2R3B plays a major role in regulating the crucial replication origins firing sys tem. “This means its study could change the paradigm of cancer therapy. So, clearly, we want to better characterize these X-chromo some-related pathways in cancer progression to be able to find innovative drugs.” ■

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