antidepressant treatment
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2022 ◽  
Author(s):  
Jan Engelmann ◽  
Lea Zillich ◽  
Josef Frank ◽  
Stefanie Wagner ◽  
Metin Cetin ◽  
...  

Abstract Although the currently available antidepressants are well established in the treatment of major depressive disorder (MDD), there is strong variability in the response of individual patients. Reliable predictors to guide treatment decisions before or in an early stage of treatment are needed. DNA-methylation has been proven a useful biomarker in different clinical conditions, but its importance for mechanisms of antidepressant response has not yet been determined. 80 MDD patients were selected out of >500 participants from the Early Medication Change (EMC) cohort with available genetic material based on their antidepressant response after four weeks and stratified into clear responders and age- and sex-matched non-responders (N=40, each). Early improvement after two weeks was analyzed as a secondary outcome. DNA-methylation was determined using the Illumina EPIC BeadChip. Epigenome-wide association studies were performed and differentially methylated regions (DMRs) identified using the comb-p algorithm. Enrichment was tested for hallmark gene-sets and in genome-wide association studies of depression and antidepressant response. No epigenome-wide significant differentially methylated positions were found for treatment response or early improvement. Twenty DMRs were associated with response; the strongest in an enhancer region in SORBS2, which has been related to cardiovascular diseases and type II diabetes. Another DMR was located in CYP2C18, a gene previously linked to antidepressant response. Results pointed towards differential methylation in genes associated with cardiac function, neuroticism, and depression. Linking differential methylation to antidepressant treatment response is an emerging topic and represents a step towards personalized medicine, potentially facilitating the prediction of patients’ response before treatment.


2022 ◽  
Vol 12 ◽  
Author(s):  
Lei Zhao ◽  
Donglin Wang ◽  
Shao-Wei Xue ◽  
Zhonglin Tan ◽  
Hong Luo ◽  
...  

Deficits in emotion regulation are the main clinical features, common risk factors, and treatment-related targets for major depressive disorder (MDD). The neural bases of emotion regulation are moving beyond specific functions and emphasizing instead the integrative functions of spatially distributed brain areas that work together as large-scale brain networks, but it is still unclear whether the dynamic interactions among these emotion networks would be the target of clinical intervention for MDD. Data were collected from 70 MDD patients and 43 sex- and age-matched healthy controls. The dynamic functional connectivity (dFC) between emotion regions was estimated via a sliding-window method based on resting-state functional magnetic resonance imaging (R-fMRI). A k-means clustering method was applied to classify all time windows across all participants into several dFC states reflecting recurring functional interaction patterns among emotion regions over time. The results showed that four dFC states were identified in the emotion networks. Their alterations of state-related occurrence proportion were found in MDD and subsequently normalized following 12-week antidepressant treatment. Baseline strong dFC could predict the reduction rate of Hamilton Depression Rating Scale (HAMD) scores. These findings highlighted the state-dependent reconfiguration of emotion regulation networks in MDD patients owing to antidepressant treatment.


Biomedicines ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 56
Author(s):  
Anna Dimoula ◽  
Dimitrios Fotellis ◽  
Evmorfia Aivalioti ◽  
Dimitrios Delialis ◽  
Alexia Polissidis ◽  
...  

Depression emerges as a risk factor for cardiovascular disease, and it is thought that successful antidepressant treatment may reduce such a risk. Therefore, antidepressant treatment embodies a potential preventive measure to reduce cardiovascular events in patients with depression. Accumulating evidence indicates that antidepressants have off-target effects on vascular dysfunction and in the early stages of atherosclerosis, which form the basis for cardiovascular disease (CVD) pathogenesis. In this context, we performed a thorough review of the evidence pertaining to the effects of different classes of antidepressant medications on hemodynamic and early atherosclerosis markers. The preclinical and clinical evidence reviewed revealed a preponderance of studies assessing selective serotonin reuptake inhibitors (SSRI), whereas other classes of antidepressants are less well-studied. Sufficient evidence supports a beneficial effect of SSRIs on vascular inflammation, endothelial function, arterial stiffening, and possibly delaying carotid atherosclerosis. In clinical studies, dissecting the hypothesized direct beneficial antidepressant effect of SSRIs on endothelial health from the global improvement upon remission of depression has proven to be difficult. However, preclinical studies armed with appropriate control groups provide evidence of molecular mechanisms linked to endothelial function that are indeed modulated by antidepressants. This suggests at least a partial direct action on vascular integrity. Further research on endothelial markers should focus on the effect of antidepressants on treatment responders versus non-responders in order to better ascertain the possible beneficial vascular effects of antidepressants, irrespective of the underlying course of depression.


2021 ◽  
Vol 14 ◽  
Author(s):  
Duan Zeng ◽  
Shen He ◽  
Nan Zhao ◽  
Manji Hu ◽  
Jie Gao ◽  
...  

Based on our previous studies and other evidence, miR-124 is an important biomarker and therapeutic target for major depressive disorder (MDD). The aim of this study was to clarify the role of miR-124 methylation in MDD and antidepressant effects from the perspective of epigenetics. MethylTarget™ was used to detect methylation levels of the three miR-124 precursor genes (MIR124-1, MIR124-2, and MIR124-3) in 33 pre- and post-treatment MDD patients and 33 healthy controls. A total of 11 cytosine-phosphate-guanine (CpG) islands in the three miR-124 precursor genes, including 222 CpG sites, were detected. All CpG islands were hypomethylated in MDD patients when compared to healthy controls and seven CpG regions were still identified with a statistically significant difference after Bonferroni correction. In addition, 137 of 222 CpG sites were found a statistical difference between MDD patients and controls, and 40 CpG sites were still statistically significant after Bonferroni correction. After performing the LASSO regression model, seven biomarkers with differential methylation among 40 CpG sites were identified. Mean methylation score was lower in MDD patients (z = −5.84, p = 5.16E-9). The AUC value reached 0.917 (95% CI: 0.854–0.981) to discriminate MDD and controls. No changes in methylation of the three miR-124 precursor genes were found in MDD patients following antidepressant treatment. The methylation of miR-124 could be a promising diagnostic biomarker for MDD.


2021 ◽  
Vol 28 (1) ◽  
pp. 4-8
Author(s):  
Chloe Wigg ◽  
Sara Costi

SUMMARYThe Cochrane review by Davies et al aimed to address the lack of clarity on the risks and benefits of switching and augmentation strategies in the pharmacological treatment of treatment-resistant depression in adults who did not respond (or partially responded) to at least 4 weeks of antidepressant treatment at a recommended dose. This commentary assesses their review and their conclusion that augmenting the current antidepressant with mianserin or with an antipsychotic improves depressive symptoms over the short-term (8 to 12 weeks). Their results need to be treated with caution owing to the small body of evidence and individual comparisons supported by one, two or three studies, the limited evidence on long-term effects and the significant gaps in the literature (e.g. a lack of studies assessing dose increases).


2021 ◽  
Author(s):  
Yuji Zhan ◽  
◽  
Mengxin Rui ◽  
Wenfeng Zeng ◽  
Yunxia Wang

Review question / Objective: The aim of this meta-analysis of randomized controlled trials is to evaluate the efficacy and safety of escitalopram and agomelatine in the major depressive disorder. Condition being studied: Major depressive disorder (MDD), is one of the most common, costly, and disabling mental health conditions worldwide, with an estimated 246 million sufferers globally in 2020.At present, there is a great demand for effective antidepressant treatment in medicine. Information sources: We will search, with no time restrictions, the following databases for relevant English language literature: PubMed, the Cochrane Central Register of Controlled Trials and Web of Science. The search string will be built as follows: (escitalopram) AND (agomelatine) AND (major depressed disorder).


2021 ◽  
Vol 14 (12) ◽  
pp. 1288
Author(s):  
Anton Loonen ◽  
Taichi Ochi ◽  
Lisanne Geers ◽  
German Simutkin ◽  
Nikolay Bokhan ◽  
...  

This article develops the idea that clinical depression can be seen as a typical human response, largely rooted in human culture, to events of loss or times of adversity. Various biological, psychological, and social factors may cause some individuals to have a depressive reaction that is ineffectually limited in time and/or severity. Recovery occurs mainly based on natural resilience mechanisms, which come into play spontaneously, but which are sometimes inhibited or blocked by specific pathological biopsychosocial mechanisms. One of the mechanisms for this could be the influence of the circuits that regulate pleasure and happiness, along the dorsal diencephalic connection (DDC) pathway from the forebrain to the midbrain via the habenula. Therapy works by undermining the biopsychosocial factors that prevent the natural recovery mechanism from working. Treatment should, therefore, be seen as facilitating rather than causing natural recovery. This approach is in line with the high recovery rate after placebo treatments and the positive influence of pharmacological treatments with completely different sites of action. Acceptance of this model means that when studying new treatments for depression, a new paradigm must be applied in which the relative value of antidepressant treatment is specifically weighted in terms of enabling the natural resilience process.


2021 ◽  
Vol 12 ◽  
Author(s):  
Ines Gallego-Landin ◽  
Alba García-Baos ◽  
Adriana Castro-Zavala ◽  
Olga Valverde

Major depressive disorder is a high-impact, debilitating disease and it is currently considered the most prevalent mental illness. It is associated with disability, as well as increased morbidity and mortality. Despite its significant repercussions in our society, its exact pathophysiology remains unclear and therefore, available antidepressant treatment options are limited and, in some cases, ineffective. In the past years, research has focused on the development of a multifactorial theory of depression. Simultaneously, evidence supporting the role of the endocannabinoid system in the neurobiology of neuropsychiatric diseases has emerged. Studies have shown that the endocannabinoid system strongly impacts neurotransmission, and the neuroendocrine and neuroimmune systems, which are known to be dysfunctional in depressive patients. Accordingly, common antidepressants were shown to have a direct impact on the expression of cannabinoid receptors throughout the brain. Therefore, the relationship between the endocannabinoid system and major depressive disorder is worth consideration. Nevertheless, most studies focus on smaller pieces of what is undoubtedly a larger mosaic of interdependent processes. Therefore, the present review summarizes the existing literature regarding the role of the endocannabinoid system in depression aiming to integrate this information into a holistic picture for a better understanding of the relationship between the two.


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