DHA Deficiency and Prefrontal Cortex Neuropathology in Recurrent Affective Disorders, ,

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Abstract

Increasing evidence suggests that docosahexaenoic acid [DHA, 22:6(n-3)], the principal (n-3) fatty acid in brain gray matter, has neurotrophic and neuroprotective properties. Preliminary clinical evidence also suggests that the perinatal accrual, and the subsequent dietary maintenance of, cortical DHA is positively associated with cortical gray matter volumes. The pathophysiology of recurrent affective disorders, including unipolar and bipolar depression, is associated with (n-3) fatty acid deficiency, DHA deficits, impaired astrocyte mediated vascular coupling, neuronal shrinkage, and reductions in gray matter volume in the prefrontal cortex (PFC). Preclinical studies have also observed neuronal shrinkage and indices of astrocyte pathology in the DHA-deficient rat brain. Together, this body of evidence supports the proposition that DHA deficiency increases vulnerability to neuronal atrophy in the PFC of patients with affective disorders. Because projections from the PFC modulate multiple limbic structures involved in affective regulation, this represents one plausible mechanism by which (n-3) fatty acid deficiency may increase vulnerability to recurrent affective disorders.

Abbreviations used:

DHA
docosahexaenoic acid
EPA
eicosapentaenoic acid
MDD
major depressive disorder
OFC
orbitofrontal cortex
PFC
prefrontal cortex

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1

Published as a supplement to The Journal of Nutrition. Presented as part of the symposium entitled “DHA and Neurodegenerative Disease: Models of Investigation” given at the Experimental Biology 2009 meeting, April 19, 2009, in New Orleans, LA. This symposium was sponsored the ASN and supported by an unrestricted educational grant from Martek Bioscience. The symposium was chaired by Jay Whelan and Robert K. McNamara. Guest Editor for this symposium publication was Cathy Levenson. Guest Editor disclosure: no conflicts to disclose.

2

Supported in part by National Institute of Mental Health grant MH083924.

3

Author disclosure: R. K. McNamara received funding from Martek Biosciences Inc., the Inflammation Research Foundation, Janssen Ortho-McNeil Pharmaceuticals, and NIH/National Institute of Mental Health.