Abstract

Evidence from human studies indicates that maternal metabolic state and malnutrition dramatically influence the risk for developing psychiatric complications in later adulthood. In this regard, the central role of polyunsaturated fatty acids (PUFAs), and particularly n-3 PUFAs, is emerging considering that epidemiological evidences have established a negative correlation between n-3 PUFA consumption and development of mood disorders. These findings were supported by clinical studies indicating that low content of n-3 PUFAs in diet is linked to an increased susceptibility to psychiatric disorders. PUFAs regulate membrane fluidity and exert their central action by modulating synaptogenesis and neurotrophic factor expression, neurogenesis, and neurotransmission. Moreover, they are precursors of molecules implicated in modulating immune and inflammatory processes in the brain. Importantly, their tissue concentrations are closely related to diet intake, especially to maternal consumption during embryonal life, considering that their synthesis from essential precursors has been shown to be inefficient in mammals. The scope of this review is to highlight the possible mechanisms of PUFA functions in the brain during pre- and post-natal period and to evaluate their role in the pathogenesis of psychiatric diseases.

Highlights

  • Maternal malnutrition has been linked to the development of different neuropsychiatric disorders in infancy (Autism Spectrum Disorder (ASD)) [1], in childhood (Attention deficit disorder (ADHD)) [2]ref, in adolescence (Schizophrenia spectrum disorders (SSD)) [3,4] or in adulthood [5]

  • In searching for dietary factors that may be linked to the development of these neuropsychiatric disorders, the role of polyunsaturated fatty acids (PUFAs) is becoming more evident considering that the analysis of lipid composition, the-so called lipidomics, is gaining great attention in psychiatric illness field [6]

  • Very recently it has been demonstrated that glucocorticoid receptors (GR) functioning is altered only in an area crucially involved in emotional behavior, such as prefrontal cortex (PFC), of mice exposed to poor n-3 PUFA diet from conception, further supporting the major role of these lipids in cortical maturation [120]

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Summary

Introduction

Maternal malnutrition has been linked to the development of different neuropsychiatric disorders in infancy (Autism Spectrum Disorder (ASD)) [1], in childhood (Attention deficit disorder (ADHD)) [2]. Neurotrophic factor expression [49] These lipids are essential to assure proper brain n-3 PUFAs have been reported to exert their central action by modulating synaptogenesis and functioning considering that DHA contentthese is higher than any other tissue [50]. When diets are poor in n-3 PUFAs, endoreticulum, as well as peroxisomes, metabolically produce n-6 derivatives, namely n-6 docosapentaenoic acid (22:5n-6), whose insertion into biological membranes, in place of DHA, is considered the main process responsible of CNS dysfunction [11]. AA, are precursors of important molecules, the eicosanoids, involved in inflammation and immune system regulation In this regard, high n-6 PUFA consumption during early development and during infancy has been associated with an increased risk of allergic syndromes indicating that these lipids may play a role in programming of immune system [70]. Either epidemiological or preclinical, are indicating the deleterious effects that low maternal consumption of n-3 PUFA may have in offspring, in relation to psychiatric disorders

Early Life Programming
Role of n-3 PUFAs on Depression and Anxiety
Role of Maternal n-3 PUFAs on Schizophrenia Spectrum Disorders
Role of n-3 PUFAs on Autistic Spectrum Disorders
Role of n-3 PUFAs on Attention Deficit Disorder
Findings
Conclusions
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