Impact Factor


Front. Aging Neurosci., 11 July 2013 | http://dx.doi.org/10.3389/fnagi.2013.00026

Brain injury, neuroinflammation and Alzheimer's disease

  • 1Regenerative Medicine Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA
  • 2Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA
  • 3Department of Physiology and Biophysics, Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA, USA

With as many as 300,000 United States troops in Iraq and Afghanistan having suffered head injuries (Miller, 2012), traumatic brain injury (TBI) has garnered much recent attention. While the cause and severity of these injuries is variable, severe cases can lead to lifelong disability or even death. While aging is the greatest risk factor for Alzheimer's disease (AD), it is now becoming clear that a history of TBI predisposes the individual to AD later in life (Sivanandam and Thakur, 2012). In this review article, we begin by defining hallmark pathological features of AD and the various forms of TBI. Putative mechanisms underlying the risk relationship between these two neurological disorders are then critically considered. Such mechanisms include precipitation and ‘spreading’ of cerebral amyloid pathology and the role of neuroinflammation. The combined problems of TBI and AD represent significant burdens to public health. A thorough, mechanistic understanding of the precise relationship between TBI and AD is of utmost importance in order to illuminate new therapeutic targets. Mechanistic investigations and the development of preclinical therapeutics are reliant upon a clearer understanding of these human diseases and accurate modeling of pathological hallmarks in animal systems.

Keywords: traumatic brain injury, Alzheimer disease, neuroinflammation, chronic traumatic encephalopathy, tauopathy, amyloid-beta peptides, neuronal loss, transgenic rat model

Citation: Breunig JJ, Guillot-Sestier M-V and Town T (2013) Brain injury, neuroinflammation and Alzheimer's disease. Front. Aging Neurosci. 5:26. doi: 10.3389/fnagi.2013.00026

Received: 04 April 2013; Paper pending published: 24 April 2013;
Accepted: 13 June 2013; Published online: 11 July 2013.

Edited by:

Orly Lazarov, The University of Illinois at Chicago, USA

Reviewed by:

Karl Herrup, Case Western University, USA
Jiawei Zhou, Shanghai Institutes for Biological Sciences Chinese Academy of Sciences, China

Copyright © 2013 Breunig, Guillot-Sestier and Town. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.

*Correspondence: Joshua J. Breunig, Regenerative Medicine Institute at Cedars-Sinai Medical Center, Advanced Health Sciences Pavilion Building Room A8109, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA e-mail: joshua.breunig@cshs.org;
Terrence Town, Department of Physiology and Biophysics, Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, 1501 San Pablo Street, Los Angeles, CA 90089-2821, USA e-mail: ttown@usc.edu

These authors have contributed equally to this work.