Targeting inflammation to influence cognitive function following spinal cord injury: a randomized clinical trial

• Published in: Spinal cord Vol. 55; no. 1; pp. 26 - 32
• Main Authors: Allison, D J, Josse, A R, Gabriel, D A, Klentrou, P, Ditor, D S
• Format: Journal Article
• Language: English
• Published: England Nature Publishing Group 01.01.2017
• Subjects: Adult; Aged; Biomarkers - blood; Cognition - physiology; Female; Humans; Kynurenine - metabolism; Learning - physiology; Male; Mental Recall - physiology; Middle Aged; Neuroimmunomodulation - physiology; Neuropsychological Tests; Spinal Cord Injuries - diet therapy; Spinal Cord Injuries - immunology; Spinal Cord Injuries - psychology; Time Factors; Treatment Outcome; Young Adult
• ISSN: 1362-4393; 1476-5624
• DOI: 10.1038/sc.2016.96

This study was a randomized, parallel-group, controlled clinical trial. The purpose of this study was to examine the efficacy of targeting inflammation as a means of improving cognitive function in individuals with spinal cord injury. Participants were recruited from the Niagara region of Ontario Canada and all testing occurred on-site at Brock University. Indices of memory and verbal learning were assessed by means of the California Verbal Learning Test (CVLT). Inflammation and concentrations of neuroactive compounds related to the kynurenine pathway were assessed via a number of pro- and anti-inflammatory cytokines, as well as tryptophan, kynurenine and several large neutral amino acids. All assessments were performed at baseline as well as at 1 month and 3 months during a 3-month intervention by means of an anti-inflammatory diet. Despite a reduction in inflammation, all measures of the CVLT, including list A, trial 1 (P=0.48), learning slope (P=0.46), long delay free recall (P=0.83), intrusions (P=0.61) and repetitions (P=0.07), showed no significant group × time interaction. It may be possible that the reduction in inflammation achieved in the current study was insufficient to induce substantial changes in indices of verbal learning and memory. Alternatively, as these participants likely underwent years of previous chronic inflammation, the underlying hippocampal damage may have negated potential improvements induced by acute reductions in inflammation.