John MacDonald, Scientist
Why I Became a Scientist
Curiosity! When I was growing up I became highly interested in psychiatry as espoused by Freud and others. Abnormal behaviour begs the question of what is the mechanism of “normal” human behaviour. Although I was fascinated by the Freudian anecdotal approaches to analyzing behaviour it made me realize that there had to be a better more scientific approach to the mind. The advent of biopsychiatry and the use of drugs to treat major mental illnesses struck me as a confirmation of the experimental scientific method as the most valid approach to understanding and treating mental illness. My curiosity for understanding actual mechanisms of brain function lead me to a career in studying neurons and synapses at the most basic level.
Research Summary
Providing new types of pharmacological therapy for Canadians facing Stroke and Alzheimer's disease is likely the most important concern for maintaining quality of life for an aging population. With covert strokes and in age-related degenerative diseases, brain cells are lost and the ability of these cells to communicate information is impaired. Consequentially, deficits of learning and memory and in thinking abilities in general result. Alzheimer's disease is a major example characterized by changes in excitatory communication between brain cells. The MacDonald laboratory is using molecular, electrophysiological and behavioural approaches to understand the mechanisms responsible for these problems. Several critical ion channel proteins including NMDAR, TRPM2 and TRPM7 are correlated with damage in strokes, with aging and with the degenerative mechanisms underlying Alzheimer's. They are using this basic information to design potential clinical therapies for preventing the loss of function and cells in Stroke and Alzheimer’s disease.
Research Questions and Disease Implications
Education
1975 PhD, Physiology and Neuroscience, University of British Columbia
Training
Post-doctoral Fellowships:
1975 Medical Research Council of Canada, University of St. Andrews, United Kingdom
1976 Medical Research Council of Canada, McGill University, Montreal
1978 Fogarty International, National Institutes of Health, Bethesda, Maryland
Publications
Wen-Li Wei, Hong-Shuo Sun, Michelle E. Olah, Xiujun Sun Elzbieta Czerwinska, Waldemar Czerwinski,
Yasuo Mori, Beverley A. Orser, Zhi-Gang Xiong, Michael F. Jackson, Michael Tymianski and John F.
MacDonald, TRPM7 Channels in Hippocampal Neurons Detect Levels of Extracellular Divalent Cations,
In press. Proceedings of the National Academy of Science U.S.A., 2007.
Xiong ZG, Zhu XM, Chu XP, Minami M, Hey J, Wei WL, MacDonald JF, Wemmie JA, Price MP, Welsh
MJ, Simon RP. Neuroprotection in ischemia: blocking calcium-permeable acid-sensing ion channels. Cell.
2004 Sep 17;118(6):687-98.
Aarts, M, Iihara, K, Li, W, Xiong, Z, Arundine, M, MacDonald, JF, and Tymianski, M. On the mechanism
of Anoxic Neuronal Death: TRPM7 as a final common pathway. Cell Dec 26; 115(7): 863-77 2003.
Suhas A. Kotecha and MacDonald, J.F. Co-stimulation of mGluR5 and NMDA receptors is required for
potentiation of excitatory synaptic transmission in hippocampal neurons. Journal of Biological Chemistry,
Jul 25; 278(30): 27742-9 2003.
Contact Information
Dr. John MacDonald
Robarts Research Institute
P.O. Box 5015, 100 Perth Drive
London, ON Canada N6A 5K8
E-Mail: jfmacdonald@robarts.ca
Heidi Van Galen
Executive Assistant
Phone: 519-931-5255
Email: hvangalen@robarts.ca