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Robert McDonald, PhD
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Affiliation(s):
University of Lethbridge; Department of Neuroscience; Canadian Center for Behavioural Neuroscience
Areas of Interest:
age-related cognitive decline, etiology of sporadic version of Alzheimer's disease, rodent models of AD, multiple co-factor models, circadian rhythm dysfunction, cholinergic depletions, mini-strokes, seizure activity, stress, beta-amyloid
Biography & Research:
Dr. McDonald received his PhD from McGill University. His first academic position was held at the University of Toronto for 10 years and he was awarded tenure. He took a Canada Research Chair position at the Canadian Center for Behavioural Neuroscience at the University of Lethbridge in 2004 and is currently a Board of Governors Research Chair in Neuroscience (Tier 1).
The foundation of his research program has been directed at understanding the organization of learning and memory function in the mammalian brain. He has been a major proponent of multiple memory systems theory and developed ideas about how these systems might interact to produce thought and behaviour.
In addition to this work, his research team has been developing alternative animal models of the etiology of the sporadic form of Alzheimer’s disease (AD). The dominant etiological theories posit that genetic mutations cause protein malformations and accumulations in the brain that result in brain dysfunction and memory impairments associated with AD. This may be the cause of the rare familial version of AD but 90% of people that get AD have the sporadic form of which the cause is not known. Despite these facts, most of the funding and biomedical research has been directed at models of the familial version. He has proposed that this brain disease can manifest itself as a result of various combinations of co-factors (McDonald, 2002). An individual Alzheimer’s patient would have some combination of these factors but the type and combinations could be different from another patient with similar clinical symptoms. These different combinations of co-factors would trigger different mechanisms of brain dysfunction and require treatments targeting those specific mechanisms. He has completed various “proof of principle” experiments showing that combining factors linked to AD produce significant hippocampal-based learning and memory impairments and hippcampal dysfunction.
Since the mid-90s McDonald's research team has been investigating the effects of circadian disruption (CD) on learning and memory function. They were the first to show that photoperiod shifting had no effect on acquisition or short-term retention of spatial memories but did impair long-term retention. This work suggested that hippocampal memory consolidation processes are particularly vulnerable to circadian manipulations. They have also assessed the effects of short versus long-term photoperiod shifting showing more global brain dysfunction in areas involved in cognitive functions following long bouts of CD. Importantly, females were protected from these effects. Finally, they have also been investigating the role of CD in aging to dementia and Alzheimer’s disease.