Omega-3 fatty acids and monoamine neurotransmission

BanI polymorphism of cytosolic phospholipase A2 gene and somatic symptoms in medication-free acute depressed patients

“…In addition, changes in the n-3 to n-6 PUFAs ratio may affect monoamine neurotransmission [45], and possibly increase the risk of developing depression [46] and somatic symptoms. Thus, the balance between the n-3 PUFAs and n-6 PUFAs may be crucial in manifestation of somatic symptoms in depression.…”

Tissue-specific Functions in the Fatty Acid-binding Protein Family

“…Studies with HFABP-null mice have shown that HFABP expression is necessary to maintain the 6/3-PUFA balance in adult brain cells and that decreased HFABP expression lowers the incorporation of AA into brain PLs, in particular phosphatidylinositol (23). An imbalance in the 6/3 ratio of brain membranes is thought to be a factor in the pathogenesis of several neurological and psychiatric disorders (24), and decreased HFABP expression is found in the brains of patients with Down syndrome and Alzheimer disease, providing indirect evidence of a connection between HFABP and neurological function (25)(26)(27).…”

“…An increase in BFABP expression is directly correlated with DHA utilization, and BFABP-null mice display decreased DHA incorporation into PLs, with an increase in AA and PA incorporation (3). Interestingly, BFABP expression levels are increased in schizophrenia, bipolar disorder, and Down syndrome and have been associated with increased anxiety and depression and altered emotional behavior (3,25); these disorders are proposed to be linked to 3-PUFA deficiency via alterations in dopaminergic and serotonergic processes (24).…”

Post-Myocardial Infarction Depression

“…The influence of PUFA omega-3 on psychiatric disorders has yielded mechanistic hypotheses, one of which involves the anti-inflammatory properties of fatty acids, in accordance with the fact that increased cytokine levels are associated with depression (Orr and Bazinet 2008;Kiecolt-Glaser 2010). A second hypothesis, based on PUFA omega-3 depletion studies, involves a modulation of monoaminergic neurotransmission (Chalon 2006) since a profound PUFA omega-3 deficiency is able to alter several neurotransmission systems such as dopaminergic and serotonergic. PUFA omega-3 may also improve depression via an anti-apoptotic neuroprotective mechanism.…”