The Reminder is making its archives back to 2003 available on our website. Please note that, due to technical limitations, archive articles are presented without the usual formatting.
TORONTO Ð A team of researchers led by scientists at The Hospital for Sick Children has discovered that the mammalian gene, p73 is essential for protecting the brain through the normal aging process. The findings suggest that reduced levels of p73 may increase a personÕs likelihood of developing AlzheimerÕs or another neurodegenerative disorder. Their findings are published in the September 2008 issue of Neuron. Using mouse models, researchers determined that a genetic variation that causes insufficiency for p73 leads to behavioural and anatomical changes commonly observed in the aging brain. Decreased levels of p73 were also found to cause key hallmarks of AlzheimerÕs disease, namely the appearance of deposits that resemble tangles, which are thought to interfere with and impair thinking and memory. ÒThese findings are particularly exciting because little is known about why and how the brain ages or develops a disease like AlzheimerÕs,Ó says Dr. David Kaplan, a co-lead author of the study. ÒBy showing the previously unsuspected role that p73 plays in neurodegeneration, we are one step closer to unraveling this mystery,Ó adds Dr. Freda Miller, the studyÕs other co-lead author. These findings could eventually lead to the development of genetic tests that measure levels of the gene and help determine whether a person is at enhanced risk for developing AlzheimerÕs. Early detection of this genetic anomaly in children could lead to therapies to address the issue before it manifests itself later in life. Other possibilities could include the development of drugs that increase the levels of p73, potentially helping to delay or halt the progression of neurodegenerative disease and aging. The AlzheimerÕs Society of Canada estimates that 450,000 (or one in 13) Canadians over the age of 65 have AlzheimerÕs or similar degenerative brain diseases.