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Article

Persistent Infiltration and Impaired Response of Peripherally-Derived Monocytes after Traumatic Brain Injury in the Aged Brain

1
Brain and Spinal Injury Center, University of California, San Francisco, CA 94143, USA
2
Department of Physical Therapy Rehabilitation Science, University of California, San Francisco, CA 94143, USA
3
Department of Neurological Surgery, University of California, San Francisco, CA 94143, USA
4
Weill Institute for Neuroscience, University of California, San Francisco, CA 94158, USA
5
Kavli Institute of Fundamental Neuroscience, University of California, San Francisco, CA 94158, USA
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2018, 19(6), 1616; https://doi.org/10.3390/ijms19061616
Received: 30 April 2018 / Revised: 21 May 2018 / Accepted: 25 May 2018 / Published: 30 May 2018
(This article belongs to the Special Issue Molecular Research on Neurodegenerative Diseases)
Traumatic brain injury (TBI) is a leading cause for neurological disabilities world-wide. TBI occurs most frequently among the elderly population, and elderly TBI survivors suffer from reduced recovery and poorer quality of life. The effect of age on the pathophysiology of TBI is still poorly understood. We previously established that peripherally-derived monocytes (CCR2+) infiltrate the injured brain and contribute to chronic TBI-induced cognitive deficits in young animals. Furthermore, age was shown to amplify monocyte infiltration acutely after injury. In the current study, we investigated the impact of age on the subchronic response of peripherally-derived monocytes (CD45hi; CCR2+) and their role in the development of chronic cognitive deficits. In the aged brain, there was a significant increase in the number of peripherally-derived monocytes after injury compared to young, injured animals. The infiltration rate of peripherally-derived monocytes remained elevated subchronically and corresponded with enhanced expression of CCR2 chemotactic ligands. Interestingly, the myeloid cell populations observed in injured aged brains had impaired anti-inflammatory responses compared to those in young animals. Additionally, in the aged animals, there was an expansion of the blood CCR2+ monocyte population after injury that was not present in the young animals. Importantly, knocking out CCR2 to inhibit infiltration of peripherally-derived monocytes prevented chronic TBI-induced spatial memory deficits in the aged mice. Altogether, these results demonstrate the critical effects of age on the peripherally-derived monocyte response during the progression of TBI pathophysiology. View Full-Text
Keywords: traumatic brain injury; monocyte; inflammation; ageing; cognition traumatic brain injury; monocyte; inflammation; ageing; cognition
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MDPI and ACS Style

Chou, A.; Krukowski, K.; Morganti, J.M.; Riparip, L.-K.; Rosi, S. Persistent Infiltration and Impaired Response of Peripherally-Derived Monocytes after Traumatic Brain Injury in the Aged Brain. Int. J. Mol. Sci. 2018, 19, 1616. https://doi.org/10.3390/ijms19061616

AMA Style

Chou A, Krukowski K, Morganti JM, Riparip L-K, Rosi S. Persistent Infiltration and Impaired Response of Peripherally-Derived Monocytes after Traumatic Brain Injury in the Aged Brain. International Journal of Molecular Sciences. 2018; 19(6):1616. https://doi.org/10.3390/ijms19061616

Chicago/Turabian Style

Chou, Austin, Karen Krukowski, Josh M. Morganti, Lara-Kirstie Riparip, and Susanna Rosi. 2018. "Persistent Infiltration and Impaired Response of Peripherally-Derived Monocytes after Traumatic Brain Injury in the Aged Brain" International Journal of Molecular Sciences 19, no. 6: 1616. https://doi.org/10.3390/ijms19061616

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