McMaster University

McMaster University

Angela L. Scott,

PhD

Assistant Professor
Pathology and Molecular Medicine

Division: Anatomy

McMaster University
1R1D Health Sciences Centre
scottan@mcmaster.ca

 

Scott

Faculty Biography

Education and Professional Standing

FRAXA Postdoctoral Fellow, McMaster University, 2015

NSERC Postdoctoral Fellow, McMaster University, 2012

EMBO Postdoctoral Fellow, University of Edinburgh, 2010

PhD, Department of Zoology, University of British Columbia, 2009

BA, Department of Psychology, University of Saskatchewan, 2003

BSc, Department of Physiology, University of Saskatchewan, 2002


Interests

Disorders of the nervous system are one of the leading causes of disability within Canada. Elucidation of the dynamic molecular and cellular relationships that govern development and neuroplasticity within the nervous system is at the heart of understanding the underlying causes and advancing therapeutic strategies. My research lies in uncovering the inter- and intra-cellular activity driving neuroplasticity and elucidating the molecular mechanisms that govern these interactions during development or neurological stress. While neurons provide the essential wiring within the nervous system, glial cells are responsible for a myriad of functions that determine the quality, maintenance, and re-growth of lost connections. I am particularly fascinated by the ever-expanding roles discovered for glial cells in regulating basic neural physiology, and examine these in respect to three main themes:

1) Neurodevelopmental Disorders

Here, we focus on a subset of glial cells, the astrocytes, which are intimately associated with neurons during development and at localized points of neuronal connections. Our current work examines how changes in astrocyte physiology and signalling underscore the abnormal neural circuitry in developmental diseases, such as Fragile X Syndrome (Autism Spectrum Disorder).

2) Neurological Stress

In response to physiological stress, the mammalian nervous system undergoes either adaptive or maladaptive changes that determine the level of recovery or tolerance of the system. Characterizing glial physiology under extreme conditions is a key component of understanding these changes and functional consequences. One of the most common stresses with devastating consequences in the nervous system is hypoxia (low levels of oxygen), which results from an array of conditions, including: trauma, damage or a blockage of blood vessels, developmental abnormalities to vasculature, fetal and prenatal complications, or environmental conditions. I am particularly interested in the role of astrocytes in these conditions given their close association with blood vessels and oxygen sensitivity. Understanding the interplay between the vasculature, glial and neuronal cells during periods of hypoxia has broad implications to neurological injury and recovery.

3) Adaptive Neuroplasticity

In an effort to understand the molecular and cellular mechanisms governing adaptive neuroplasticity, we use comparative model species that have adapted to extreme neurological conditions. Our investigations include model species such as zebrafish, a highly regenerative and hypoxia tolerant species; as well as high-altitude deer mice, a mammalian model of hypoxia adaptation. These models offer great insight into novel mechanisms of neuroplasticity and the cellular and molecular factors driving adaptive responses.

Academic Interests

Dr. Scott is currently involved in teaching within the Education Program in Anatomy. She teaches Neuroanatomy in the Undergraduate Medical Program within the Faculty of Health Sciences.  


Team Members

(Fall, 2017)


Graduate Student:

Rida Malik (MSc)

Undergraduate Students:

Amanda Poxon (4th year thesis)

Chloe Wong (4th year thesis)

David Shin (3rd year project)

Selected Publications

  • Altered developmental expression of the astroctye-secreted factors Hevin and SPARC in the Fragile X mouse model. Wallingford, J., Scott, A., Rodrigues, K., and Doering, L. Submitted for publication.
  • Hypoxia-regulated catecholamine secretion of chromaffin cells. Nurse, C., Salman, S., and Scott, A. Submitted for publication.
  • Disregulation of purinergic signalling and alterations in astrocyte physiology in Fragile X Syndrome. Scott, A., Wong, C., Chen, A., and Doering, L. Publication in progress.
  • Adaptations to hypoxia-induced stress responses in high-altitude deer mice (Peromyscus maniculatus). Scott, A., Pranckevicius, N., Patal, P., and Scott, G. Publication in progress.
  • The role of astrocytes in the developing brain. Scott, A. and Doering, L. (2016) International Innovation. (www.internationalinnovation.com/role-astrocytes-developingbrain/)
  • Enhanced BDNF signalling following chronic hypoxia potentiates catecholamine release from adrenal chromaffin cells. Scott, A., Zhang, M. and Nurse, C. (2015) Journal of Physiology 593 (15): 3281-3299.
  • Serotonin promotes regeneration of motor neurons, but not serotonergic interneurons in the spinal cord of adult zebrafish. Barreiro-Iglesias, A.*, Mysiak, K.*, Scott, A. *(co-first author), Reimer, M., Becker, C., and Becker, T.  (2015) Cell Reports 13 (5): 924-932.
  • Dopamine from the brain promotes spinal motor neuron generation during development and adult regeneration. Reimer, M., Norris, A., Ohnmacht, J., Patani, R., Zhong, Z., Dias, T., Kuscha, V., Scott, A., Chen, Y., Rozov, S., Frazer, S., Wyatt, C., Higashijima, S., Patton, E., Panuala, P., Chandran, S., Becker, T., and Becker, C. (2013) Developmental Cell 25(5): 478-91.
  • "Neurotrophins in Axonal Regeneration and Myelination." In: Handbook of Neurotoxicity: Neurotrophins. Springer, Heildelberg. (2012) Bedard, S., Scott, A., and Ramer, M.
  • Molecular evolution of cytochrome c oxidase underlies high-altitude adaptation in the bar-headed goose. Scott, G., Schulte, P., Egginton, S., Scott, A., Richards, J., Milsom, W. (2011) Molecular Biology and Evolution 28(1): 351-63.
  • A new organellar complex in rat sympathetic neurons. Ramer, M., Cruz Cabrera, M., Alan, N., Scott, A., and Inskip, J. (2010) PLoS ONE 5(5): e1000872.
  • Differential regulation of dendritic plasticity by neurotrophins following deafferentation of the adult spinal cord is independent of p75NTR. Scott, A. and Ramer, M. (2010) Brain Research 1323: 48-58.
  • Depletion of spinal 5-HT promotes mechanosensory recovery in the deafferented spinal cord. Cragg, J., Scott, A. and Ramer, M. (2010) Experimental Neurology 222(2): 277-84.
  • Schwann cell p75NTR prevents spontaneous sensory re-innervation of the adult spinal cord. Scott, A. and Ramer, M. (2010) Brain 133 (2): 421-32.
  • Is inhibition of axonal regeneration by astrocytes in the dorsal part of the spinal cord regulated by p75 receptor? Scott, A. and Ramer, M. (2010) Brain 133 (6): e145.
  • Targeting myelin to optimize plasticity of spared axons in the denervated spinal cord. Scott, A.*, Ramer, L.* (co-first author), Soril, L., Kwiecien, J., and Ramer, M. (2006) Molecular Neurobiology 33(2): 91-111.
  • Deafferentation and neurotrophin-mediated intraspinal sprouting: a central role for the p75 neurotrophin receptor. Scott, A., Borisoff, J., and Ramer, M. (2005) European Journal of Neuroscience 21(1): 81-92.

Valid XHTML 1.0 Transitional Level Double-A conformance, W3C WAI Web Content Accessibility Guidelines 2.0