Abstract
n-3 and n-6 polyunsaturated fatty acids (PUFAs) are essential fatty acids that are provided by dietary intake. Growing evidence suggests that n-3 and n-6 PUFAs are paramount for brain functions. They constitute crucial elements of cellular membranes, especially in the brain. They are the precursors of several metabolites with different effects on inflammation and neuron outgrowth. Overall, long-chain PUFAs accumulate in the offspring brain during the embryonic and post-natal periods. In this review, we discuss how they accumulate in the developing brain, considering the maternal dietary supply, the polymorphisms of genes involved in their metabolism, and the differences linked to gender. We also report the mechanisms linking their bioavailability in the developing brain, their transfer from the mother to the embryo through the placenta, and their role in brain development. In addition, data on the potential role of altered bioavailability of long-chain n-3 PUFAs in the etiologies of neurodevelopmental diseases, such as autism, attention deficit and hyperactivity disorder, and schizophrenia, are reviewed.
Highlights
A team showed in mice that KO of sterol regulatory element-binding proteins (Srebps)-1c induced an alteration of GABAergic transmission, leading to symptoms similar to schizophrenia: hyperactivity, depression-like symptoms, and social deficits [103]. All these results show that SREBP-1 could play a role in synaptic plasticity and transmission via the regulatory loop with n-3 Polyunsaturated fatty acids (PUFAs)
The mechanisms underlying the deleterious effect of both prenatal dietary n-3 PUFA deficiency and inflammatory stimulus on later-life behavior have started to be understood; for example, the exacerbated production of inflammatory factors in the embryonic brain could disturb brain wiring [247], the microglia phagocytic activity of spines, leading to excessive pruning [248] and/or microbiota disturbance [246], which has been reported to be involved in neurodevelopmental disorders [249,250]
(BTBR mouse strain), dietary deficiency in n-3 PUFAs from gestation to early adulthood induced developmental delay and altered sociability [297]. These results were observed when these animals were fed with dietary n-3 PUFAs supplementation [297], suggesting that LC n-3 PUFAs cannot counterbalance the social deficits induced by such a genetic inbreeding
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Fads: fatty acid desaturase; elovl: elongase; EPA: eicosapentaenoic acid; ARA: arachidonic acid; the n-6 (cyan) and n-3 (orange) families Polymorphisms in those genes (SNPs) are associated with variations of plasma. Fads: fatty acid desaturase; elovl: elongase; EPA: eicosapentaenoic acid; ARA: arachidonic acid; DHA: addition to their crucial role in the structure and function of cell membranes, n-3 docosahexaenoic acid; ALA: α-linolenicInacid; LA: linoleic acid; DPA: docosapentaenoic acid; D5D: delta-5 desaturase; D6D: and n-6 PUFAs are substrates for the production of several signaling molecules involved delta-6 desaturase; Elovl: elongasein5;the. EPA, DHA, and ARA are hydrolyzed by the specific phospholipase A2 (PLA2) and can be further In addition to their crucial role in the structure and function of cell membranes, n-3 and n-6 PUFAs are substrates for the production of several signaling molecules involved in the physiological function of the cells, especially in the brain [1,7]. We will discuss the potential role of these PUFAs in neurodevelopmental disorders, focusing on autism spectrum disorders (ASD), attention deficit and hyperactivity disorder (ADHD), and schizophrenia
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
