A team of researchers led by The Hospital for Sick Children (SickKids), the University of Toronto (U of T) and Cold Spring Harbor Laboratory have discovered a protein that is responsible for shaping the nervous system. This research was made possible with the support of a $1.5-million NeuroScience Canada Brain Repair ProgramTM team grant that enabled scientists from across Canada to work together and fast track their research. This research is reported in the December 8, 2005 issue of the journal Neuron.

"We discovered that p63 is the major death-promoting protein for nerve cells during fetal and post-natal development," said Dr. David Kaplan, the paper's senior author, senior scientist at SickKids, professor of Molecular Genetics, Medical Genetics & Microbiology at U of T, Canada Research Chair in Cancer and Neuroscience, and co-team leader on the NeuroScience Canada Brain Repair Program grant with Dr. Freda Miller of SickKids. "Proteins such as p63 that regulate beneficial cell death processes during development may cause adverse affects later in life by making us more sensitive to injury and disease."

At birth, the nervous system has twice the number of nerve cells than needed. The body disposes of the excess cells by eliminating those that go to the wrong place or form weak or improper connections. If this process does not happen, the nervous system cannot function properly. The expression of the p63 protein guides the nervous system in disposing of the ineffective nerve cells. The protein is from the p53 family of tumour suppressor proteins that is mutated in many human cancers.

While p63 is involved in determining which nerve cells die, the research team also suspects that it determines whether nerve cells die when injured or in neurological and neurodegenerative diseases such as Alzheimer's and Parkinson's diseases.

"The discovery of this new protein represents hope for thousands of people affected by neurological and neuro
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Contact: Chelsea Gay
chelsea.gay@sickkids.ca
416-813-5045
University of Toronto
7-Dec-2005

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