Improved Working Memory but No Effect on Striatal Vesicular Monoamine Transporter Type 2 after Omega-3 Polyunsaturated Fatty Acid SupplementationReportar como inadecuado

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Studies in rodents indicate that diets deficient in omega-3 polyunsaturated fatty acids n–3 PUFA lower dopamine neurotransmission as measured by striatal vesicular monoamine transporter type 2 VMAT2 density and amphetamine-induced dopamine release. This suggests that dietary supplementation with fish oil might increase VMAT2 availability, enhance dopamine storage and release, and improve dopamine-dependent cognitive functions such as working memory. To investigate this mechanism in humans, positron emission tomography PET was used to measure VMAT2 availability pre- and post-supplementation of n–3 PUFA in healthy individuals. Healthy young adult subjects were scanned with PET using 11C-+-α-dihydrotetrabenzine DTBZ before and after six months of n–3 PUFA supplementation Lovaza, 2 g-day containing docosahexaenonic acid, DHA 750 mg-d and eicosapentaenoic acid, EPA 930 mg-d. In addition, subjects underwent a working memory task n-back and red blood cell membrane RBC fatty acid composition analysis pre- and post-supplementation. RBC analysis showed a significant increase in both DHA and EPA post-supplementation. In contrast, no significant change in 11CDTBZ binding potential BPND in striatum and its subdivisions were observed after supplementation with n–3 PUFA. No correlation was evident between n–3 PUFA induced change in RBC DHA or EPA levels and change in 11CDTBZ BPND in striatal subdivisions. However, pre-supplementation RBC DHA levels was predictive of baseline performance i.e., adjusted hit rate, AHR on 3-back on the n-back task y = 0.19+0.07, r2 = 0.55, p = 0.009. In addition, subjects AHR performance improved on 3-back post-supplementation pre 0.65±0.27, post 0.80±0.15, p = 0.04. The correlation between n-back performance, and DHA levels are consistent with reports in which higher DHA levels is related to improved cognitive performance. However, the lack of change in 11CDBTZ BPND indicates that striatal VMAT2 regulation is not the mechanism of action by which n–3 PUFA improves cognitive performance.

Autor: Rajesh Narendran , William G. Frankle, Neale S. Mason, Matthew F. Muldoon, Bita Moghaddam



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