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Neural Dynamics Research Group

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Our Mission

      The Neural Dynamics Research Group is dedicated to determining the causes
and stages in the progression of various neurological diseases that occur at different periods in life.  These include developmental disorders of the nervous system, such as ASD, as well as age-dependent disorders of later life (ALS, Parkinson’s disease, Alzheimer’s disease).  We believe that our current model systems approach, as well as additional methods under development, will allow us to achieve these goals.  We hope to use the  knowledge derived from these models to push for translational medical approaches to preventing or halting neurological diseases before the underlying pathological mechanisms of action have done irreparable harm to the nervous system. Our ultimate goal is to prevent neurodegenerative diseases across the lifespan.


History of the laboratory by Dr. Chris Shaw


      I started the laboratory in Ophthalmology in 1988 upon moving from Dalhousie to UBC. At that time the lab was called the 'Receptor Lab' due to the research focus on the role of various neurotransmitter receptors in neuroplasticity of visual cortex with a focus on the early critical period. The lab had just begun moving from the characterization of receptors frozen tissue to studies focusing on living tissue. Much of the early work of the laboratory was devoted to justifying the new techniques and providing data that the 'in vitro living slice' could be used to characterize receptors. Once this was done, we
shifted our focus to a series of studies of functional regulation of such receptors in response to biological stimulation. In turn, the studies of regulation led to studies of the mechanisms underlying regulation, i.e. the activation of various protein kinases and phosphatases, the ions controlling such activation, etc. By this time, my students and I had begun to realize
that the process of receptor regulation was very dynamic: neural activity changes caused receptor regulation, in turn altering neural activity and so on. This realization had a profound impact on our thinking about plasticity processes in the developing and adult nervous system. It also had implications for understanding neurological disease. These thoughts led to
the editing of my first book, "Receptor Dynamics in the Nervous System' (1996). During this period we had a secondary focus on the role of glutathione in the brain and the possibility that glutathione could be a neurotransmitter. These studies culminated with the second book, "Glutathione in the Nervous System" (1998).


      The next major stage of laboratory development came when we began to collaborate with various clinical researchers on ALS. Initially, these were simple receptor assays on frozen material but the studies gradually expanded
to examine protein kinase and phosphatase activities as well. To our surprise, we found that molecules affected by disease were the same as those involved in neuroplastic modifications of neurons. This observation led to the notion that plasticity and pathology are closely related mechanistically via a continuum of events. These observations were the basis for a series of review articles dealing with long-term potentiation, epilepsy, and pathology. Ultimately, these articles formed the basis for the third edited volume (with co-editor, Jill McEachern), "Toward a Theory of Neuroplasticity" (2000)


      Continuing with our studies of degenerative diseases of the nervous system, especially ALS, I became aware of an odd neurological disorder on the island of Guam. This disease, ALS-parkinsonism dementia complex (ALS-PDC) showed a
number of remarkable features that had led early investigators, notably Dr. LT Kurland, to describe it as a neurological Rosetta Stone. Key features were its incredibly high incidence, the incidence at earlier ages than seen
outside of Guam, and often grouping of clinical and pathological features of ALS, parkinsonism, and Alzheimer's disease. The strongest epidemiological link was to the consumption of the seed of the cycad plant that  contained a neurotoxin. Surprisingly, no one had previously developed an animal model of ALS-PDC in order to test this hypothesis. Our immediate
goal became that of developing such a model system of the disease in order to assess the causal stages of neuronal degeneration. To do so, the lab had to shift focus on a number of fronts. First, we changed from a predominant
focus on receptor assays to the study of a number of crucial molecules involved in neurodegeneration. Next, we began to learn how to conduct behavioral assessments of function in mice. At about this time the laboratory moved from its previous 'home' in the Department of Anatomy (UBC campus) to its current location at the Research Pavilion, VGH. At the same
time, our official name changed to the Neural Dynamics Research Group, reflecting a general change in our outlook and focus on neurological diseases and plasticity.


      These efforts in developing a mouse model of ALS-PDC have shown spectacular success and have rewarded us with what we believe are crucial insights into the role of environmental toxins as key factors in neurological disease, and
some important molecular events that lead to neural cell death. The skills the lab has acquired along the way in various other projects are all utilized to further probe the model. This model with its potential to provide a detailed understanding of the causes and progression of neurodegeneration has become the lab's sole focus and main effort. In consequence of this model and its successful development, our grant funding has increased significantly, and with this additional funding have come new faces and outlooks (See current projects under Research link).


       Most recently we have broadened our focus to look at other neurotoxins that may contribute to neurological disorders in different phases of life.  One of the toxins we are now examining both in vitro and in vivo is aluminum which is well known for its neurotoxic potential.  Our current studies are looking at both dietary and injection routes of delivery of aluminum at different ages.  The goal is to model both the features of late onset neurological disorders such as those we have previously worked on (ALS, PD, AD), but also to examine the impacts of aluminum in earlier life.  In regard to the latter, we are attempting to model aspects of autism spectrum disorder (ASD), the latter which correlates with a high degree of significance in humans with the number of aluminum-adjuvanted vaccines administered in early life.