Is depression associated with increased oxidative stress? A systematic review and meta-analysis

Black, Catherine N.; Bot, Mariska; Scheffer, P; Cuijpers, Pim; Penninx, Brenda W. J. H.

doi:10.1016/j.psyneuen.2014.09.025

Cited by 591 publications

(403 citation statements)

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“…With every double bond, a fatty acid becomes exponentially more susceptible (Assies et al 2014). Of note, many psychiatric disorders manifest themselves together with an increase in oxidative stress, defined as an imbalance between increased free radical formation on the one hand, and decreased anti-oxidant defense on the other (Maes et al 2009;Assies et al 2014;Black et al 2015). This may lead to interesting interactions with fatty acid metabolism (Assies et al 2014) as discussed below.…”

Section: Oxidative Stress Vulnerabilitymentioning

confidence: 99%

Focus on fatty acids in the neurometabolic pathophysiology of psychiatric disorders

Mocking

Assies

Ruhé

et al. 2018

J of Inher Metab Disea

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Continuous research into the pathophysiology of psychiatric disorders, such as major depressive disorder (MDD), posttraumatic stress disorder (PTSD), and schizophrenia, suggests an important role for metabolism. This narrative review will provide an upto-date summary of how metabolism is thought to be involved in the pathophysiology of these psychiatric disorders. We will focus on (I) the important role of fatty acids in these metabolic alterations, (II) whether fatty acid alterations represent epiphenomena or risk factors, and (III) similarities and dissociations in fatty acid alterations between different psychiatric disorders. (Historical) epidemiological evidence links fatty acid intake to psychiatric disorder prevalence, corroborated by altered fatty acid concentrations measured in psychiatric patients. These fatty acid alterations are connected with other concomitant pathophysiological mechanisms, including biological stress (hypothalamic-pituitary-adrenal (HPA)-axis and oxidative stress), inflammation, and brain network structure and function. Metabolomics and lipidomics studies are underway to more deeply investigate this complex network of associated neurometabolic alterations. Supplementation of fatty acids as disease-modifying nutraceuticals has clinical potential, particularly add-on eicosapentaenoic acid (EPA) in depressed patients with markers of increased inflammation. However, by interpreting the observed fatty acid alterations as partly (mal)adaptive phenomena, we attempt to nuance translational expectations and provide new clinical applications for these novel neurometabolic insights, e.g., to predict treatment response or depression recurrence. In conclusion, placing fatty acids in context can contribute to further understanding and optimized treatment of psychiatric disorders, in order to diminish their overwhelming burden of disease.

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Section: Oxidative Stress Vulnerabilitymentioning

confidence: 99%

Focus on fatty acids in the neurometabolic pathophysiology of psychiatric disorders

Mocking

Assies

Ruhé

et al. 2018

J of Inher Metab Disea

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“…Recent studies reported decreased BDNF and increased glia-derived neurotrophic factor (GDNF) levels in both mania and depression (17), increased GDNF/BDNF ratio in mania (18), and increased GDNF levels during manic switch due to ECT (19) confirming the role of the disrupted supportive cellular network in BD. Altered antioxidant enzymes, lipid peroxidation and nitric oxide levels (20)(21)(22), as well as increased DNA damage (23)(24)(25)(26)(27) in BD and a probable coactivation of oxidative damage and repair mechanisms have been reported, particularly in a depressive state of BD (28). Also various inflammatory markers such as TNF-α, interleukin (IL) 1β, IL-6, IL-10, IL-18, IL-4, interferon-γ, monocyte chemotactic protein-1, fibroblast growth factor β, vascular endothelial growth factor, and hs-CRP were reported to be activated in both manic and depressive states of BD (29,30).…”

mentioning

confidence: 99%

Bipolar bozuklukta allostaz ve allostatik yükü yeniden değerlendirmek

Özerdem¹

2015

Dusunen Adam

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“…Alterations in glutathione homeostasis that lead to greater oxidative stress have been implicated in a range of neuropsychiatric and neurodegenerative diseases, including cognitive impairment (Zhao & Zhao, 2013;Baierle et al, 2015;Black et al, 2015). Furthermore, increased oxidative stress can lead to an elevated stress response, and stimulation of apoptosis pathways, resulting in 'sick' cells and ultimately cell death (Townsend et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

The role of adult vitamin D deficiency in cognition and brain function in mice

Groves¹

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Vitamin D deficiency is prevalent throughout the world. Even in a temperate climate such as Australia, one-third of the adult population has insufficient levels of serum vitamin D (25-hydroxyvitamin D levels <50 nmol/L). Epidemiological studies have shown significant associations between vitamin D deficiency and an increased risk of various neuropsychiatric and neurodegenerative disorders, such as schizophrenia, depression, Alzheimer's disease and cognitive impairment. However, studies based on observational epidemiology cannot address questions of causality; they cannot determine if vitamin D deficiency is a causal factor leading to the adverse health outcome. The use of animal experiments can examine the biological plausibility of the relationship between vitamin D deficiency and adverse brain outcomes.Vitamin D is a neurosteroid that has a wide range of functions within the brain including calcium maintenance, regulation of neurotrophic factors, neurogenesis, and neuroprotection. Using a model of adult vitamin D (AVD) deficiency in BALB/c mice, we have previously shown alterations in a range of behaviours and an imbalance between excitatory and inhibitory neurotransmission, which may be relevant to a range of neuropsychiatric disorders. Therefore, we have provided experimental evidence demonstrating that vitamin D deficiency in adulthood impacts on a range of brain functions, and is therefore a biologically plausible risk factor for the development of neuropsychiatric disorders. However, there is currently insufficient evidence to account for the mechanism(s) by which this occurs.There were four main aims of the thesis; to determine whether AVD deficiency impacts on (1) cognition, (2) adult hippocampal neurogenesis, and (3) glutamate and GABA signaling in BALB/c mice; and to determine if AVD deficiency would (4) exacerbate the effects of a secondary exposure, in this case social stress, in BALB/c mice and in the more resilient C57BL/6J mice.To address these aims I assessed attentional processing in BALB/c mice using the 5 choice serial reaction time task and found sex-dependent impairments in AVD-deficient male mice only.Structural and diffusion tensor imaging was assessed using MRI in male mice, however we found no significant alterations in gross brain structure or connectivity within the brain in the group exposed to AVD deficiency. I used immunohistological techniques to assess two measures of hippocampal neurogenesis, cell proliferation and survival of newborn neurons, and found that hippocampal neurogenesis was not affected by AVD deficiency at baseline or following wheel running stimulated neurogenesis.iii Despite no cellular level change in neurogenesis, the analysis of the proteomics of the hippocampus, although preliminary, provided clues that AVD deficiency may have an effect on synapse formation and plasticity, and dendritic arborisation and that these changes may be responsible for impaired learning and memory. The proteomics also provided convergent evidence of an effect on glutamate and...

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Is depression associated with increased oxidative stress? A systematic review and meta-analysis

Abstract: This meta-analysis finds that oxidative stress, as measured by 8-OHdG and F2-isoprostanes, is increased in depression. Larger-scale studies are needed to extend the evidence on oxidative stress in depression, and examine the potential impact of treatment.

Cited by 591 publications

References 67 publications

Focus on fatty acids in the neurometabolic pathophysiology of psychiatric disorders

Focus on fatty acids in the neurometabolic pathophysiology of psychiatric disorders

Bipolar bozuklukta allostaz ve allostatik yükü yeniden değerlendirmek

The role of adult vitamin D deficiency in cognition and brain function in mice

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