QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Rapoport, S. I. Search for Related Content PubMed PubMed Citation Articles by Rapoport, S. I.

---

Symposium: Dietary PUFA and the Aging Brain—Food for Thought

Arachidonic Acid and the Brain^1–3,

Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892

Kinetic methods in unanesthetized rodents have shown that turnover rates of arachidonic acid (AA) and docosahexaenoic acid (DHA) in brain membrane phospholipids are rapid and energy consuming and that phospholipase A₂ (PLA₂) and acyl-CoA synthetase enzymes that regulate turnover are specific for one or the other PUFA. Thus, AA turnover in brain phospholipids was reduced, and AA-selective cytosolic cPLA₂ or acyl-CoA synthetase, as well as cyclooxygenase (COX)-2, were downregulated in brains of rats given drugs effective against bipolar disorder, whereas DHA turnover and expression of DHA-selective calcium-independent iPLA₂ were unchanged. Additionally, the brain AA and DHA cascades can be altered reciprocally by dietary or genetic conditions. Thus, following 15 wk of dietary (n-3) PUFA deprivation, DHA loss from rat brain was slowed because of reduced iPLA₂ and COX-1 expression, whereas AA-selective cPLA₂, sPLA₂, and COX-2 were upregulated, as were AA and docosapentaenoic acid concentrations. Measured rates of AA and DHA incorporation into brain represent their respective rates of metabolic consumption, because these PUFA are not synthesized de novo or converted significantly from their precursors in brain. In healthy human volunteers, positron emission tomography (PET) was used to show that the brain consumes AA and DHA at respective rates of 17.8 and 4.6 mg/d, whereas in patients with Alzheimer disease, AA consumption is elevated. In the future, PET could be used to relate human brain rates of AA and DHA consumption to liver PUFA metabolism and dietary PUFA intake.

^* To whom correspondence should be addressed. E-mail: sir{at}helix.nih.gov.

This article has been cited by other articles:

				C. B. Divito and S. G. Amara Close Encounters of the Oily Kind: Regulation of Transporters by Lipids Mol. Interv., October 1, 2009; 9(5): 252 - 262. [Abstract] [Full Text] [PDF]

				W. J. Lukiw and N. G. Bazan Docosahexaenoic Acid and the Aging Brain J. Nutr., December 1, 2008; 138(12): 2510 - 2514. [Abstract] [Full Text] [PDF]

				J. Whelan (n-6) and (n-3) Polyunsaturated Fatty Acids and the Aging Brain: Food for Thought J. Nutr., December 1, 2008; 138(12): 2521 - 2522. [Abstract] [Full Text] [PDF]