Phone:
709-864-4955 (office)
709-864-4953 (lab)


Email:
craig.moore@mun.ca

Address:
H5339 - Division of BioMedical Sciences
Faculty of Medicine, Memorial University of Newfoundland
300 Prince Philip Drive
St. John's, NL
CANADA A1B 3V6

Research Interests: Neuroimmunology, inflammation, glial cell biology, extracellular vesicles, microRNAs and multiple sclerosis

Summary of Research: The rates of brain-related diseases in Canada and the developed world are rising—not only among older adults, but also among those aged 18 to 45. In this younger group, the most common neurological disease is multiple sclerosis (MS). Unfortunately, current treatments for MS target the immune system and have little or no effect on the brain. My lab is currently investigating how new biomarkers and potential drug targets can drive the brain’s own repair processes. Furthermore, my lab aims to identify specific genes and microRNAs responsible for promoting both brain injury and repair processes in patients with MS and other chronic neurodegenerative diseases.

For a full list of publications and scope of my research interests, click here.

Current Research Projects

1) MicroRNA-related research: MicroRNAs (miRNAs) are small, highly conserved non-coding RNA molecules that are involved in endogenous mRNA silencing and post-transcriptional regulation of gene expression. In the central nervous system (CNS), each major cell type has a distinct miRNA signature (termed miRNAome). As a consequence, the differential expression of miRNAs contributes to the unique expression of proteins, thereby influencing overall phenotype and function. Upon disruption of homeostasis, expression profiles of miRNAs are rapidly altered, leading to changes in the expression of proteins within a particular cell. Therefore, miRNAs play critical roles in fundamental cellular processes, and both directly and indirectly influence the complex CNS environment. our long-term objective is to better understand how specific miRNA molecules can impact the overall fate and function of CNS cells. Achieving these specific objectives will further elucidate the role of miRNAs as regulators of glial and neuronal cell function.

Relevant publications:

D.A. Galloway, S.J. Carew, S.N. Blandford, N. Fudge, T. Berry, G.R.W. Moore, J. Barron, and C.S. Moore. Investigating the NLRP3 inflammasome and its regulator mir-223-3p in multiple sclerosis and experimentally-induced demyelination. J. Neurochem. 2022 May 28. https://pubmed.ncbi.nlm.nih.gov/35633501/

D.A. Barnes, D.A. Galloway, M. Hoener, M.D. Berry, and C.S. Moore. TAAR1 expression in human macrophages and brain tissue: a potential novel facet of MS neuroinflammation. Int. J. Mol. Sci. 2021; Oct 27;22(21):11576. https://pubmed.ncbi.nlm.nih.gov/34769007/

D.A. Galloway, S. Blandford, T. Berry, J.B. Williams, M. Stefanelli, M. Ploughman, C.S. Moore. Mir-223 Promotes Regenerative Myeloid Cell Phenotype and Function in the Demyelinated Central Nervous System. Glia. 2019 May;67(5):857-869. https://pubmed.ncbi.nlm.nih.gov/30548333/

D.A Galloway and C.S. Moore. miRNAs as Emerging Regulators of Oligodendrocyte Development and Differentiation. Frontiers Cell Devel. Biol. 2016 Jun 17;4:59. https://pubmed.ncbi.nlm.nih.gov/27379236/

C.S. Moore, V. Rao, B.A. Durafourt, B.J. Bedell, S.K. Ludwin, A. Bar-Or, J.P. Antel. Mir-155 as a multiple sclerosis-relevant regulator of myeloid cell polarization. Annals of Neurology 2013 Nov;74(5):709-20. https://pubmed.ncbi.nlm.nih.gov/23818336/

2) Extracellular vesicle (EV) and biofluid biomarker-related research: Extracellular vesicles (EVs) are a heterogenous population of phospholipid bilayer particles that are released from all cells, and are comprised of exosomes, microvesicles, and apoptotic bodies. Since these different particles are defined by their biogenesis and difficult to distinguish, the broader term of ‘EVs’ has been widely adopted by researchers. EVs are highly stable, cross the blood-brain-barrier, and contain molecular cargo, including proteins, lipids, mRNAs, and miRNAs that can be trafficked to recipient cells. In the CNS, both neurons and glia release EVs that help guide neural development and maintain homeostasis. While blood and CSF-derived EVs have been suggested as biomarkers that can also influence cell function, the EV-cargo itself is likely the key factor driving cellular responses. In diseases of the CNS, including MS, EVs derived from endothelial, immune, and CNS cells have all been measured in the blood and/or CSF and investigated as potential biofluid biomarkers. In addition to EVs, my lab also investigates other potential biofluid biomarkers and their pathophysiological roles related to promoting inflammation and repair in the CNS.

Relevant publications:

S.N. Blandford, N.J. Fudge, and C.S. Moore. CXCL10 Is Associated with Increased Cerebrospinal Fluid Immune Cell Infiltration and Disease Duration in Multiple Sclerosis. Biomolecules 2023; 13,8;1204.  https://pubmed.ncbi.nlm.nih.gov/37627269/

S.N. Blandford, N.J. Fudge, C. Corkum and C.S. Moore. Analysis of plasma using flow cytometry reveals increased lymphocyte-derived extracellular vesicles in stable untreated relapse remitting multiple sclerosis. Front. Immunol. 2022 Mar 22;13:803921. https://pubmed.ncbi.nlm.nih.gov/35392085/

S.N. Blandford, D.A. Galloway, J.B. Williams, S. Arsenault, J. Brown, G. MacLean, G.R.W. Moore, J. Barron, M. Ploughman, F. Clift, M. Stefanelli, and C.S. Moore. Interleukin-1 receptor antagonist: An exploratory biomarker that correlates with disability and provides pathophysiological insights in relapsing-remitting multiple sclerosis. Multiple Sclerosis Relat. Disorders 2021 Jul;52:10300. https://pubmed.ncbi.nlm.nih.gov/34004435/

S.N. Blandford, D.A. Galloway, and C.S. Moore. The Roles of Extracellular Vesicle MicroRNAs in the Central Nervous System. Glia. 2018 Nov;66(11):2267-2278. https://pubmed.ncbi.nlm.nih.gov/29726599/

3) Basic and fundamental neuroimmunology-related research: Research within the biomedical sciences not only can relate to further elucidating cellular and molecular mechanisms related to various diseases, but can also aim to better understand basic fundamental concepts related to how different cells within the human body communicate under homeostatic states. Research performed in my lab investigates the fundamental cellular and molecular mechanisms responsible for influencing glial cell phenotypes, function, and inter-cellular communication with the immune and central nervous systems. Specifically, my lab is interested in identifying species- and cell-specific differences, and how altered bioenergetic profiles within cells of myeloid-origin are influenced by cell activation.

Relevant publications:

E. Nutma, N. Fancy, M. Weinert, M.C Marzin, S. Tsartsalis, R.C.J. Muirhead, I. Falk, J. deBruin, D. Hollaus, R. Pieterman, J. Anink, D. Story, S. Chandran, J. Tang, M.C. Trolese, T. Saito, T.C. Saido, K. Wiltshire, P. Beltran-Lobo, A. Philips, J. Antel, L. Healy, D.A. Galloway, R.Y. Benoit, C. Bendotti, E. Aronica, C.I. Radulescu, S.J. Barnes, D.W. Hampton, P. vanderValk, S. Jacobson, P.M. Matthews, C.S. Moore*, S. Amor*, and D.R. Owen*.  Translocator protein is an activator of microglia in rodent models but not human neurodegenerative diseases. Nature Communications 2023 Aug 28;14(1):5247. https://pubmed.ncbi.nlm.nih.gov/37640701/

D.A. Barnes, M. Hoener, C.S. Moore, and M.D. Berry. TAAR1 regulates purinergic-induced TNF secretion from peripheral, but not CNS resident macrophages. J. Neuroimmun Pharm 2023 Jun;18(1-2):100-111. https://pubmed.ncbi.nlm.nih.gov/36380156/

D.A. Galloway, A.E.M Phillips, D.R.J. Owen, C.S. Moore. Phagocytosis in the Brain: Homeostasis and Disease. Front. Immunology. 2019 Apr 16;10:790. https://pubmed.ncbi.nlm.nih.gov/31040847/

D.A. Galloway, J.B. Williams, and C.S. Moore. Effects of Fumarates on Inflammatory Human Astrocyte Responses and Oligodendrocyte Differentiation. Annals Clinical and Translational Neurology. 2017 May 4;4(6):381-391. https://pubmed.ncbi.nlm.nih.gov/28589165/

D.R. Owen, N. Narayan, L. Wells, L.M. Healy, E. Smyth, E.A. Rabiner, D. Galloway, J.B. Williams, J. Lehr, H. Mandhair, L.A.N. Peferoen, P.C. Taylor, S. Amor, J.P. Antel, P.M. Matthews, and C.S. Moore. Pro-inflammatory activation of primary microglia and macrophages increases 18kDa Translocator Protein (TSPO) expression in rodents but not human. J. Cerebral Blood Flow and Metabol. 2017 Aug;37(8):2679-2690. https://pubmed.ncbi.nlm.nih.gov/28530125/

M. Michell-Robinson, H. Touil, L. Healy, B.A. Durafourt, D.R. Owen, A. Bar-Or, J.P. Antel, and C.S. Moore. Roles of Microglia in Brain Development, Tissue Maintenance, and Repair. Brain 2015 May;138(Pt 5):1138-59. https://pubmed.ncbi.nlm.nih.gov/25823474/

C.S. Moore, Q.L. Cui, N. Warsi, B.A. Durafourt, N. Zorko, D.R. Owen, J.P. Antel and A. Bar-Or. Direct and Indirect Effects of Immune and Central Nervous System-Resident Cells on Human Oligodendrocyte Progenitor Cell Differentiation. Journal of Immunology 2015 Jan 15;194(2):761-72. https://pubmed.ncbi.nlm.nih.gov/25505283/

O. Butovsky, M.P. Jedrychowski, C.S. Moore, R. Cialic, A.J. Lanser, G. Gabriely, T. Koeglsperger, B. Dake, P.M. Wu, C.E. Doykan, Z. Fanek, L. Liu, Z. Chen, J.D. Rothstein, R.M. Ransohoff, S.P. Gygi, J.P. Antel, H.L. Weiner. Identification of a unique TGFb-dependent molecular and functional signature in microglia. Nature Neurosci. 2014 Jan;17(1):131-43. https://pubmed.ncbi.nlm.nih.gov/24316888/

C.S. Moore, R. Milner, A. Nishiyama, R.F. Frausto, D.R. Serwanski, R.R. Pagarigan, J.L Whitton, R.H. Miller, S.J. Crocker. Astrocytic TIMP-1 Promotes Oligodendrocyte Differentiation and Enhances CNS Myelination. J Neurosci. 2011. Apr 20;31(16):6247-54. https://pubmed.ncbi.nlm.nih.gov/21508247/