our greatest blessings come to us by way of madness Phaedr. 244a

2012/09/12

Dietary therapy to promote neuroprotection in chronic spinal cord injury


Journal of Neurosurgery: Spine

Aug 2012 / Vol. 17 / No. 2 / Pages 134-140
ARTICLE

Dietary therapy to promote neuroprotection in chronic spinal cord injury

1Department of Neurosurgery, David Geffen School of Medicine at UCLA; and 2Department of Integrative Biology and Physiology, University of California, Los Angeles, California
Abbreviations used in this paper: AdV-BDNF = adenovirusmediated BDNFBDNF = brain-derived neurotrophic factorCSM = cervical spondylotic myelopathyCur = curcuminDHA = docosahexaenoic acidSCI = spinal cord injuryWD = Western diet4-HNE = 4-hydroxynonenal.
Address correspondence to: Langston T. Holly, M.D., Department of Neurosurgery, David Geffen School of Medicine at UCLA, Center for the Health Sciences, Box 956901, Los Angeles, California 90095-6901. email: .
Please include this information when citing this paper: published online June 26, 2012; DOI: 10.3171/2012.5.SPINE1216.

Abstract


OBJECT
The pathogenesis of cervical spondylotic myelopathy (CSM) is related to both primary mechanical and secondary biological injury. The authors of this study explored a novel, noninvasive method of promoting neuroprotection in myelopathy by using curcumin to minimize oxidative cellular injury and the capacity of omega-3 fatty acids to support membrane structure and improve neurotransmission.

METHODS
An animal model of CSM was created using a nonresorbable expandable polymer placed in the thoracic epidural space, which induced delayed myelopathy. Animals that underwent placement of the expandable polymer were exposed to either a diet rich in docosahexaenoic acid and curcumin (DHA-Cur) or a standard Western diet (WD). Twenty-seven animals underwent serial gait testing, and spinal cord molecular assessments were performed after the 6-week study period.

RESULTS
At the conclusion of the study period, gait analysis revealed significantly worse function in the WD group than in the DHA-Cur group. Levels of brain-derived neurotrophic factor (BDNF), syntaxin-3, and 4-hydroxynonenal (4-HNE) were measured in the thoracic region affected by compression and lumbar enlargement. Results showed that BDNF levels in the DHA-Cur group were not significantly different from those in the intact animals but were significantly greater than in the WD group. Significantly higher lumbar enlargement syntaxin-3 in the DHA-Cur animals combined with a reduction in lipid peroxidation (4-HNE) indicated a possible healing effect on the plasma membrane.

CONCLUSIONS
Data in this study demonstrated that DHA-Cur can promote spinal cord neuroprotection and neutralize the clinical and biochemical effects of myelopathy.