The Role of Oxidative Stress in Depressive Disorders

Michel, Tanja Maria; Pülschen, D; Thome, Johannes

doi:10.2174/138161212803523554

Cited by 206 publications

(75 citation statements)

References 101 publications

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“…2011), and conversely that antioxidants have antidepressant properties (Berk et al 2008, Scapagnini et al 2012). The increasing evidence showed antioxidant effects of antidepressants and the relevance of intracellular oxidative pathways in the pathophysiology of major depression (Michel et al 2007, Maes et al 2009b, Maes et al 2011, Behr et al 2012, Michel et al 2012). A few antidepressants have come up as potential treatment options to reduce oxidative damage in major depression.…”

Section: Effects Of Antidepressants Against Oxidative Dna Damagementioning

confidence: 99%

DNA Damage in Major Psychiatric Diseases

et al. 2016

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Human cells are exposed to exogenous insults and continuous production of different metabolites. These insults and unwanted metabolic products might interfere with the stability of genomic DNA. Recently many studies demonstrated that different psychiatric disorders show substantially high level of oxidative DNA damage in the brain accompanied with morphological and functional alterations. It reveals that damaged genomic DNA may contribute to the pathophysiology of these mental illnesses. Here we review the role of oxidative damage and reduced antioxidant ability in some vastly studied psychiatric disorders and emphasize the inclusion of treatment options involving DNA repair. In addition, while most currently used antidepressants are based on the manipulation of the neurotransmitter regulation in managing different mental abnormalities, they are able to prevent or reverse neurotoxin-induced DNA damage. Therefore, it may be plausible to target on genomic DNA alterations for psychiatric therapies, which is of pivotal importance for future anti-psychiatric drug development.

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Section: Effects Of Antidepressants Against Oxidative Dna Damagementioning

confidence: 99%

DNA Damage in Major Psychiatric Diseases

et al. 2016

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“…The underlying mechanisms responsible for this could be that serum high ApoB levels are related to the dysfunctions of lipid peroxidation, malondialdehyde (MDA) and immune system that could been caused by oxidative stress and free radicals of depressive disorders that is associated with cognitive decline36373839. Elevated levels of MDA have been reported to adversely affect the efficiency of delayed memory in patients with depressive disorder40.…”

Section: Discussionmentioning

confidence: 99%

Serum ApoB levels in depressive patients: associated with cognitive deficits

Han

et al. 2017

Sci Rep

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Cognitive deficits have been regarded as one of the most significant clinical symptoms of depressive disorder. Accumulating evidence has shown that apolipoprotein B (ApoB) levels, which are responsible for inducing neurodegeneration, may be involved in cognitive deficits. This study examines cognitive deficits, and the correlation of serum ApoB levels with cognitive deficits of depressive disorder. 90 depressive patients and 90 healthy controls with matched age and gender were recruited. Cognition was assessed using the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS). Serum ApoB levels in depressive patients were measured by immunoturbidimetric method. Our results showed that depressive patients had lower scores of cognition including RBANS total score and subscales of language and delayed memory (all, p < 0.001) than healthy controls after controlling for the variables. The differences in cognitive functions also passed Bonferroni corrections. Serum ApoB levels were negatively correlated with delayed memory score in depressive patients (r = −0.30, p = 0.01). Furthermore, stepwise multivariate regression analysis indicated that serum ApoB levels independently contributed to delayed memory in depressive patients (t = −2.68, p = 0.01). Our findings support that serum ApoB levels may be involved in delayed memory decline in depressive patients. Depressive patients also experience greater cognitive deficits, especially in delayed memory and language than healthy controls.

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“…Another gene also upregulated was oxidation resistance 1, OXR1 , which codes for a protein that specifically protects against oxidative stress (Volkert et al, 2000). This gene may be important in mediating protection against increases in reactive oxygen species hypothesised to trigger neuronal atrophy in the brains of MDD patients (Michel et al, 2012). Consequently, both antidepressants may be activating genes important in progenitor proliferation and neuroprotection, which may be important in mediating their effects.…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic profiling of human hippocampal progenitor cells treated with antidepressants and its application in drug repositioning

et al. 2017

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Current pharmacological treatments for major depressive disorder (MDD) are ineffective in a significant proportion of patients, and the identification of new antidepressant compounds has been difficult. ‘Connectivity mapping’ is a method that can be used to identify drugs that elicit similar downstream effects on mRNA levels when compared to current treatments, and thus may point towards possible repositioning opportunities. We investigated genome-wide transcriptomic changes to human hippocampal progenitor cells treated with therapeutically relevant concentrations of a tricyclic antidepressant (nortriptyline) and a selective serotonin reuptake inhibitor (escitalopram). We identified mRNA changes common to both drugs to create an ‘antidepressant mRNA signature’. We used this signature to probe the Library of Integrated Network-based Cellular Signatures (LINCS) and to identify other compounds that elicit similar changes to mRNA in neural progenitor cells. Results from LINCS revealed that the tricyclic antidepressant clomipramine elicited mRNA changes most similar to our mRNA signature, and we identified W-7 and vorinostat as functionally relevant drug candidates, which may have repositioning potential. Our results are encouraging and represent the first attempt to use connectivity mapping for drug repositioning in MDD.

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The Role of Oxidative Stress in Depressive Disorders

Cited by 206 publications

References 101 publications

DNA Damage in Major Psychiatric Diseases

DNA Damage in Major Psychiatric Diseases

Serum ApoB levels in depressive patients: associated with cognitive deficits

Transcriptomic profiling of human hippocampal progenitor cells treated with antidepressants and its application in drug repositioning

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