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  • B.S. (UC Irvine)
  • M.Sc., Ph.D. (Hebrew U. of Jerusalem)
  • Professor
  • Ophthalmology and Visual Sciences
  • Office Phone: 604-875-4111 ext. 68373
    Lab Phone: 604-875-4111 ext. 68375
    Fax: 604-875-4376
    E-mail: cashawlab at gmail.com

    Current research interests:

    My laboratory's key focus over the last few years has been on the unusual neurological disease of Guam and the Western Pacific, ALS-parkinsonism dementia complex (ALS-PDC).  I view this disease as a kind of neurological Rosetta Stone able to unlock some of the key questions in neurological disease research.  For example: what are the causes of ALS, Parkinson's, and Alzheimer's and what are the pre-clinical stages of each?  Our approach has been to create an in vivo animal model in which we can look at behavioural changes in motor and cognitive functions, as well as systems, cellular and biochemical modifications as the disease process emerges over time.  We have identified a novel class of neurotoxins in the course of our initial studies and are now beginning to understand the toxic mechanisms of action that lead to the death of neurons in the spinal cord and brain.  The overall goal of this work is to identify key etiological factors involved in sporadic neurological disease and the early stages of the disease process.  From the first could come effective prophylaxis; from the latter, early phase treatment before irreversible damage to the CNS has been done. 

    A second theme to our work is to seek potential therapeutic agents for existing neurological disease states using the above, and other, animal models.  In particular, we are focusing our attention on progranulin, a neuroepithelial growth factor, and on a class of molecules called ginsenosides.  Preliminary data with progranulin suggests that the molecule can exert powerful neuroprotective effects and perhaps even reverse early phase neurodegeneration. 

    The last aspect of our work, and one that is still emerging, is to look at the potential for compounds such as aluminum to be neurotoxic.  We are interested in the types of aluminum compounds that can cause neurodegeneration, their route of administration, the impact of dose and duration, and the crucial but largely unexplored aspects of age and sex.  These studies are just beginning, but show great promise to help us understand the origin of neurological disorders as diverse as autism spectrum disorder and Alzheimer's disease. 


    Tasker RA, Adams-Marriott AL, Shaw CA. New animal models of progressive neurodegeneration: tools for identifying presymptomatic therapeutic targets. The EMPA Journal. (2010).

    Ryan CL, Baranowski DC, Chitramuthu BP, Malik S, Li Z, Cao M, Minotti S, D Durham HD, Kay DG, Shaw CA, Bennett HPJ, Bateman A. Progranulin is expressed within motor neurons and promotes neuronal cell survival. BMC Neuroscience. doi.10.1186/1471-2202-10-130. (2009).

    Shaw CA, Pelech S, Ly PTT. Paradoxical responses to neurotoxic glycosides: insights from a cellular model of ALS-PDC. Neurobiology of Lipids. 8,1 (2009).

    Shaw CA and Petrik MS. Aluminum hydroxide injections lead to motor deficits and motor neuron degeneration. J Inorganic Biochem. 103 (11): 1555-62. (2009).

    Snyder RL, Cruz-Aguado R, Sadilek M, Glasko D, Shaw C, Montine TJ. Lack of cerebral BMAA in human cerebral cortex. Neurology. 72 (15):1360-1361. (2009).

    Ly PTT, Pelech S, Shaw CA. Cholesteryl glucoside stimulates activation of protein kinase B/Akt in motor neuron-derived NSC34 cell line. Neurobiology of Lipids. 7, 4. (2008).

    Shaw CA Höglinger GU. Neurodegenerative diseases: neurotoxins as sufficient etiologic agents? J Neuromolecular Medicine. 10(1): 1-9. (2008).

    Tabata RC, Wilson JMB, Van Kampen JM, Cashman N, Shaw CA. Dietary sterol glucosides are neurotoxic to motor neurons and induce an ALS-PDC phenotype. J Neuromolecular Medicine. 10(1): 24-39. (2008).

    Petrik MS, Wilson JMB, Grant SC, Blackband SJ, Tabata RC, Shan X, Krieger C, Shaw CA. Magnetic resonance microscopy and immunohistochemistry of the CNS of the mutant SOD murine model of ALS reveals widespread neural deficits. J Neuromolecular Medicine. 9(3): 216-229, (2007).

    Ly PTT, Singh S, Shaw CA. Novel environmental toxins: steryl glucosides as a potential etiological factor for age-related neurodegenerative diseases. J Neurosci. Res. 85(2): 231-237. (2007).

    Petrik MS, Wong MC, Tabata RC, Garry RF, Shaw CA. Aluminum adjuvant linked to Gulf War illness induces motor neuron death in mice. J Neuromolecular Medicine 9: 83-100. (2007).

    Wilson, J.M.B., Khabazian, I., Wong, M.C., Seyedalikhani, A., Bains, J.S., Pasqualotto, B.A., Williams, D.E., Andersen, R.J., Simpson, R.J., Smith, R., Craig, U.K., Kurland, L.T., and Shaw, C.A. Behavioral and neurological correlates of ALS-parkinsonism dementia complex in adult mice fed washed cycad flour. J. Neuromol. Med. 1(3): 207-222. (2002).

    Khabazian, I., Bains, J. S., Williams, D.E., Cheung, J., Wilson, J.M.B., Pasqualotto, B.A., Pelech, S.L., Andersen, R.J., Wang, Y.-T., Liu, L., Nagai, A., Kim, S.U., Craig, U.-K., Shaw, C.A. Isolation of various forms of sterol b-d-glucoside from the seeds of cycas circinalis: neurotoxicity and implications for ALS-PDC. J. Neurochem. 82: 1-13. (2002).




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