CC-BY-NC-ND 4.0 · Curr Res Concussion 2017; 04(01): e38-e54
DOI: 10.1055/s-0037-1606836
Original Article
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Selective Reduction of Brain Docosahexaenoic Acid after Experimental Brain Injury and Mitigation of Neuroinflammatory Outcomes with Dietary DHA

Christopher M. Butt1, Jordan L. Harrison2, 3, 4, Rachel K. Rowe3, 4, 5, Jacob Jones6, Kelly M. Wynalda1, Norman Salem Jr.7, Jonathan Lifshitz2, 3, 4, 5, James R. Pauly6
  • 1Translational Biology, DSM Nutritional Products, Boulder, Colorado
  • 2Interdisciplinary Graduate Program in Neuroscience, Arizona State University, Tempe, Arizona
  • 3Department of Child Health, University of Arizona College of Medicine-Phoenix, Phoenix, Arizona
  • 4Barrow Neurological Institute at Phoenix Children's Hospital, Phoenix, Arizona
  • 5Phoenix VA Healthcare System, Phoenix, Arizona
  • 6Department of Pharmaceutical Sciences, Spinal Cord and Brain Injury Research Center, University of Kentucky College of Pharmacy, Lexington, Kentucky
  • 7Nutritional Lipids, DSM Nutritional Products, Columbia, Maryland
Further Information

Publication History

28 November 2016

14 August 2017

Publication Date:
29 September 2017 (online)


Background Docosahexaenoic acid (DHA) is an omega-3 fatty acid that is important for brain development and function, but the interactions of dietary DHA with fatty acid profiles, sensory sensitivities, and inflammation that may change after traumatic brain injury (TBI) are poorly understood. It is also unknown whether DHA alters experimental TBI outcomes measured more than 2 weeks after injury. The current study investigated whether dietary DHA, provided before (PreDHA) or after (PostDHA) experimental TBI, would improve outcomes for up to 24 days after injury.

Methods Rats consumed predetermined diets for 28 days prior to midline fluid percussion injury (mFPI) or to sham surgery. The effects of PreDHA, TBI, and PostDHA on comprehensive fatty acid profiles, neuroinflammation, sensory sensitivity, and spatial learning were then evaluated.

Results The results provided novel evidence that TBI selectively reduced brain DHA content, as injury did not decrease any other fatty acid that was measured. Furthermore, PreDHA and PostDHA attenuated injury-induced increases in sensory sensitivity as well as in tumor necrosis factor-α (TNF-α), interleukin-10, and interleukin-1β in the somatosensory cortex. However, [3H]PK11195 autoradiography showed that PostDHA was more effective than PreDHA in reducing microglial/macrophage activation in the somatosensory cortex, hippocampus, and substantia nigra. Spatial learning outcomes were largely unaffected by diet or injury, but PostDHA was associated with shorter swimming distances in the Morris water maze (MWM) at 15 days post-injury.

Conclusion Overall, sufficient DHA intake may be necessary to replace DHA that is lost to TBI and may improve some symptoms of post-concussive syndrome (PCS) over an extended period through inflammation-related mechanisms.

Supplementary Material