Year: 2004

Campylobacter jejuni (C. jejuni) is the leading cause of bacterial food poisoning worldwide, infecting approximately 300,000 Canadians, three million Americans, and even higher numbers in developing countries each year. Most cases result from eating contaminated poultry; other causes include exposure to young animals and drinking contaminated water or milk. The bacteria cause severe bloody diarrhea, vomiting and fever, and can lead to more serious medical problems such as bowel disease, arthritis and paralysis. Compared to well-studied bacteria like E. coli and Salmonella, relatively little is known about how C. jejuni causes disease. Using new genetic tools, Dr. Erin Gaynor is identifying and characterizing C. jejuni genes involved in causing infection. She is examining the interaction between the pathogen and host cells to determine how the bacteria cause disease at the molecular level. Dr. Gaynor is also investigating why C. jejuni causes disease in humans when it harmlessly inhabits the intestinal tracts of many other animals, and how host systems respond to infection with the bacteria. This research may lead to a greater understanding of the mechanisms of pathogenesis for C. jejuni and contribute to the development of new treatments and potentially a vaccine to prevent infection from occurring.

The causes of many brain diseases, such as epilepsy and schizophrenia, are unknown. Researchers such as Dr. Kurt Haas are exploring the possibilities that abnormal brain development in the prenatal stage may play a role. Using a powerful gene delivery technique, Dr. Haas is investigating how nerve cell activity contributes to brain development, specifically, the effect of altered levels (i.e. too much or too little) of activity on the structure and function of neuronal circuits. This research could lead to more specific and effective interventions to prevent abnormal circuits from forming during prenatal development, and also to treat adults with schizophrenia or epilepsy.

Coxsackievirus infections can cause a variety of illnesses, including heart disease. In North America, the coxsackievirus is estimated to cause up to 30 percent of new cases of dilated cardiomyopathy, a condition in which the heart becomes enlarged and pumps less strongly. Dr. Marc Horwitz is studying how viruses such as coxsackievirus can induce autoimmune diseases such as chronic heart disease, and how immune system components shape and control development of the disease. Studies have shown that the body’s immune response has a profound effect on the development of chronic heart disease after infection with the virus, revealing that immune cells and antibodies that attack infection also damage heart tissues. Dr. Horwitz is examining how innate and adaptive immune responses following viral infection contribute to development of chronic heart disease. He will use findings from the study to design and test new methods to prevent heart disease, which could also lead to new treatments.

Tumour suppressor genes, such as ING1, help regulate normal cell growth by encoding proteins that inhibit abnormal proliferation of cells. Dr. LeAnn Howe is studying the molecular properties and function of ING1 proteins to understand the processes that lead to the development and growth of tumours. Research has linked ING1 proteins to modification of histones, the main protein component of chromatin, which makes up our chromosomes and genes. Evidence suggests that defects in regulation of chromatin structure may improperly activate or silence genes, leading to disease. Dr. Howe is examining the way ING proteins interact with chromatin to determine whether the proteins can modify chromatin. This research could help explain the role of ING1 genes in cancer development and contribute to new cancer therapies.

Canada has a growing diabetes epidemic, which costs the Canadian health care system an estimated $13 billion annually. More than two million Canadians have the disease, and by 2010, the number is expected to increase to three million. Diabetes is also a major health problem worldwide. Although diabetes can be treated with insulin, a cure for this devastating disease remains elusive. All forms of diabetes are associated with the loss of functional pancreatic islet cells. However, very little is known about the underlying factors controlling how and why pancreatic islet cells die. Dr. James Johnson recently discovered important networks of molecules that control survival of islet cells. For example, one such network includes the RyR2 protein, which controls the release of calcium in the cell, and the calpain protein, which can split other proteins in response to increased calcium. Dr. Johnson is comparing the role of this survival network to other molecular networks to investigate how pancreatic islet cells die. The research could lead to better therapies for diabetes, including more successful pancreatic islet transplantation, a promising experimental treatment that depends critically on the continued survival of the donated cells. The findings could also improve understanding of other diseases where calcium is involved in cell death, such as heart failure, Alzheimer’s disease and stroke.

Parkinson’s disease is a chronic, progressive disorder that affects about 100,000 Canadians, at an annual cost of more than $2.5 billion. The disease involves loss of both brain cells and chemicals that modulate communications between brain cells – causing not only motor symptoms of tremor, stiffness, and slow movements but also cognitive and behavioural changes. Conventional drug therapy for Parkinson’s disease replaces dopamine in the brain. Although most motor deficits usually improve after therapy, more than 50 percent of patients (particularly those in the later stages of the disease) may develop difficult problems, such as involuntary movements, dementia and psychosis. Dr. Chong Lee is studying neural mechanisms of these complications, which are resulting from the disease itself or the chronic use of Parkinson’s drugs. Dr. Lee is also evaluating the effectiveness of neuro-protective treatment, a strategy to prolong the survival of injured cells and slow the progression of Parkinson’s disease. He ultimately aims to develop strategies to treat dementia and behavioural symptoms of the disease and to reduce or prevent treatment-induced complications in patients with Parkinson’s disease.