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

Chang, Jane Pei-Chen; Guu, Ta-Wei; Chen, Yi‐Chih; Gałecki, Piotr; Walczewska, Anna; Su, Kuan‐Pin

doi:10.1016/j.plefa.2017.01.001

Cited by 12 publications

(6 citation statements)

References 46 publications

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“…Interestingly, the results are also consistent with our recent findings that somatic anxiety is associated with omega-3 PUFA deficits and the genetic risks of PUFA metabolic enzyme cytosolic phospholipase A2 in major depressive disorder 62,63 and interferon α-induced neuropsychiatric syndrome. 63,64 Brain membranes contain a high proportion of omega-3 PUFAs and their derivatives and most animal and human studies suggest that a lack of omega-3 PUFAs in the brain might induce various behavioral and neuropsychiatric disorders, 16,[65][66][67][68][69][70] including anxiety-related behaviors.…”

Section: Discussionsupporting

confidence: 92%

Association of Use of Omega-3 Polyunsaturated Fatty Acids With Changes in Severity of Anxiety Symptoms

Tseng²,

Lin

et al. 2018

JAMA Netw Open

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100

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Key Points Question Is omega-3 polyunsaturated fatty acid treatment associated with an improvement in anxiety symptoms? Findings In this systematic review and meta-analysis of 19 clinical trials including 2240 participants from 11 countries, improvement in anxiety symptoms was associated with omega-3 polyunsaturated fatty acid treatment compared with controls in both placebo-controlled and non–placebo-controlled trials. The anxiolytic effects of omega-3 polyunsaturated fatty acids were also stronger in participants with clinical conditions than in subclinical populations. Meaning Omega-3 polyunsaturated fatty acid treatment for anxiety might be effective in clinical settings.

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Section: Discussionsupporting

confidence: 92%

Association of Use of Omega-3 Polyunsaturated Fatty Acids With Changes in Severity of Anxiety Symptoms

Tseng²,

Lin

et al. 2018

JAMA Netw Open

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100

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“…Moreover, it has been suggested that the genetic variations in phospholipase A2 and cyclooxygenase 2 genes, enzymes responsible for PUFAs metabolism, have been associated with the risk of inflammation-induced depression, possibly by lowering the levels of n-3 PUFAs such as EPA and DHA, which have anti-inflammatory properties, in both MDD patients [108] and medically ill patients treated with the pro-inflammatory cytokine interferon- [109]. A recently published practice guideline for clinical use of Omega-3 in Youth: ADHD, ASD and Depression 475 n-3 PUFAs in MDD [110] suggested that n-3 PUFAs in MDD treatment should be considered for special populations including pregnant women [5,[111][112][113], and children.…”

Section: Pre-clinical Studiesmentioning

confidence: 99%

Nutritional Neuroscience as Mainstream of Psychiatry: The Evidence- Based Treatment Guidelines for Using Omega-3 Fatty Acids as a New Treatment for Psychiatric Disorders in Children and Adolescents

Chang

2020

Clin Psychopharmacol Neurosci

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Omega-3 polyunsaturated fatty acids (or omega-3 PUFAs, n-3 PUFAs) are essential nutrients throughout the life span. Recent studies have shown the importance of n-3 PUFAs supplementation during prenatal and perinatal period as a potential protective factor of neurodevelopmental disorders. N-3 PUFAs have been reported to be lower in youth with attention deficit hyperactivity disorder (ADHD), autism spectrum disorder (ASD) and major depressive disorder (MDD). N-3 PUFAs supplementation has shown potential effects in the improvement of clinical symptoms in youth with ADHD, ASD, and MDD, especially those with high inflammation or a low baseline n-3 index. Moreover, it has been suggested that n-3 PUFAs had positive effects on lethargy and hyperactivity symptoms in ASD. For clinical application, the following dosage and duration are recommended in youth according to available randomized controlled trials and systemic literature review: (1) ADHD: a combination of eicosapentaenoic acid (EPA) + docosahexaenoic acid (DHA) ≥ 750 mg/d, and a higher dose of EPA (1,200 mg/d) for those with inflammation or allergic diseases for duration of 16−24 weeks; (2) MDD: a combination of a EPA + DHA of 1,000−2,000 mg/d, with EPA:DHA ratio of 2 to 1, for 12−16 weeks; (3) ASD: a combination of EPA + DHA of 1,300−1,500 mg/d for 16−24 weeks as add-on therapy to target lethargy and hyperactivity symptoms. The current review also suggested that n-3 index and inflammation may be potential treatment response markers for youth, especially in ADHD and MDD, receiving n-3 PUFA.

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“…Activation of phospholipases enhances the production of prostaglandin E2, which plays an anti-inflammatory role in the brain [ 70 ], consistent with the over-expression in MIA relative to Control pigs. Moreover, PLA2GA was over-expressed in the peripheral blood mononuclear cells in SSD compared to control individuals [ 71 ], and genetic variants of this family have been associated with depression [ 72 ]. Furthermore, also impacted by MIA were genes in the protein kinase cGMP-dependent family, including PRKG1 , PRKG2 , and PRKCB ( Table 2 ).…”

Section: Discussionmentioning

confidence: 99%

Prefrontal Cortex Response to Prenatal Insult and Postnatal Opioid Exposure

Rymut

Rund

Southey

et al. 2022

Genes

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The influence of proinflammatory challenges, such as maternal immune activation (MIA) or postnatal exposure to drugs of abuse, on brain molecular pathways has been reported. On the other hand, the simultaneous effects of MIA and drugs of abuse have been less studied and sometimes offered inconsistent results. The effects of morphine exposure on a pig model of viral-elicited MIA were characterized in the prefrontal cortex of males and females using RNA-sequencing and gene network analysis. Interacting and main effects of morphine, MIA, and sex were detected in approximately 2000 genes (false discovery rate-adjusted p-value < 0.05). Among the enriched molecular categories (false discovery rate-adjusted p-value < 0.05 and −1.5 > normalized enrichment score > 1.5) were the cell adhesion molecule pathways associated with inflammation and neuronal development and the long-term depression pathway associated with synaptic strength. Gene networks that integrate gene connectivity and expression profiles displayed the impact of morphine-by-MIA interaction effects on the pathways. The cell adhesion molecules and long-term depression networks presented an antagonistic effect between morphine and MIA. The differential expression between the double-challenged group and the baseline saline-treated Controls was less extreme than the individual challenges. The previous findings advance the knowledge about the effects of prenatal MIA and postnatal morphine exposure on the prefrontal cortex pathways.

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

Cited by 12 publications

References 46 publications

Association of Use of Omega-3 Polyunsaturated Fatty Acids With Changes in Severity of Anxiety Symptoms

Association of Use of Omega-3 Polyunsaturated Fatty Acids With Changes in Severity of Anxiety Symptoms

Nutritional Neuroscience as Mainstream of Psychiatry: The Evidence- Based Treatment Guidelines for Using Omega-3 Fatty Acids as a New Treatment for Psychiatric Disorders in Children and Adolescents

Prefrontal Cortex Response to Prenatal Insult and Postnatal Opioid Exposure

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