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Complement activation in the injured central nervous system: another dual-edged sword?

Faith H Brennan1, Aileen J Anderson2, Stephen M Taylor1, Trent M Woodruff1 and Marc J Ruitenberg13*

Author Affiliations

1 The University of Queensland, School of Biomedical Sciences, St Lucia, Brisbane, QLD, 4072, Australia

2 Anatomy & Neurobiology, University of California, Irvine, USA

3 The Queensland Brain Institute, The University of Queensland, Brisbane, QLD, 4072, Australia

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Journal of Neuroinflammation 2012, 9:137  doi:10.1186/1742-2094-9-137

Published: 21 June 2012


The complement system, a major component of the innate immune system, is becoming increasingly recognised as a key participant in physiology and disease. The awareness that immunological mediators support various aspects of both normal central nervous system (CNS) function and pathology has led to a renaissance of complement research in neuroscience. Various studies have revealed particularly novel findings on the wide-ranging involvement of complement in neural development, synapse elimination and maturation of neural networks, as well as the progression of pathology in a range of chronic neurodegenerative disorders, and more recently, neurotraumatic events, where rapid disruption of neuronal homeostasis potently triggers complement activation. The purpose of this review is to summarise recent findings on complement activation and acquired brain or spinal cord injury, i.e. ischaemic-reperfusion injury or stroke, traumatic brain injury (TBI) and spinal cord injury (SCI), highlighting the potential for complement-targeted therapeutics to alleviate the devastating consequences of these neurological conditions.