DHA
Lipids Signaling

J Stein Brain Sciences 2018 What is Developmental Dyslexia?

The high dynamic sensitivity of magnocellular neurons necessitates high membrane flexibility so that their ionic channels can open and close very fast. This flexibility is provided by their local lipid environment, particularly by the incorporation into the membrane of one very important omega 3 long chain fatty acid, Docosahexaenoic acid (DHA) [77,78]. This provides exactly the right physical and electrostatic properties for their membranes to allow optimum dynamic performance of the ionic channels passing through them [79].

Dyslexic children tend to have very low levels of DHA in their blood, and the degree of their blood DHA deficit predicts the magnitude of their reading deficit. Hence, we have found that supplementing the diet of dyslexic children with DHA can often help them to improve their reading, sometimes dramatically [80,81,82]. These observations all reaffirm the importance of magnocellular function for reading.

J Stein 2016 Nutrients. 2016 Docosahexaenoic Acid and Cognition throughout the Lifespan

Another consideration is the use of other supplements in boosting the effects of DHA, or acting in synergy, especially with regards to aging. For example, curcumin can boost DHA levels in the brain of animals [330], and it is intriguing to speculate that curcumin could help mitigate the losses in DHA that are associated with the heightened β-oxidation that is observed in AD. As previously mentioned, B vitamins and DHA work in tandem to reduce brain atrophy in MCI patients [134]. B vitamins lower Hcy, an intermediate in some oxidative stress-related pathways that are a risk factor for vascular disease as well as dementia. Hcy can also serve as notification that pathological neurodegenerative processes are occurring. Additionally, B vitamins may promote DHA incorporation into phospholipids, and likely have synergistic anti-inflammatory effects. In support of a combinatorial approach, Scheltens et al. [331] observed improvements in memory after daily supplementation with DHA, EPA, phospholipids, choline, uridine monophosphate, vitamin E, vitamin C, selenium, folic acid, vitamin B6, and vitamin B12 for 24 weeks in subjects with mild AD (Alzheimer's disease).

The non-steroidal anti-inflammatory drug (NSAID) aspirin might be another potential synergistic agent. Acetylation by aspirin enables COX-2 to initiate the biosynthetic pathway that produces resolvins (D1–D6) from DHA [332,333]. Aspirin-dependent resolvins are potent DHA-derived pro-resolving immune mediators [334]. Resolvin D3 has been shown to be especially effective in the late-resolving phase of inflammation (catabasis), the completion of which is critical to prevent an acute inflammatory response from becoming chronic activation [335]. The use of NSAIDs has been associated with a reduced risk for AD, especially in long-time users [336,337]. However, these effects are not realized in currently diagnosed AD, highlighting the likely importance of preventative supplementation [338].