Associations Among Monoamine Neurotransmitter Pathways, Personality Traits, and Major Depressive Disorder

Shao, Xiaojun; Zhu, Gang

doi:10.3389/fpsyt.2020.00381

Cited by 47 publications

(26 citation statements)

References 297 publications

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“…25 Such lesions can lead to interruption of monoaminergic pathways implicated in mood regulation. 26 Our study observed a positive association with frontal lobe lesions with PSD similar to previous studies although we did not observe a positive association with thalamic lesions. The difference observed could be due to limitations in sample size (only four thalamic strokes were observed), inaccuracies in visual assessment of the lesion (more accurate techniques of lesion analysis include: lesion segmentation, methods of brain registration to standard space, voxel-based statistics) 23 and certain strokes being excluded due to exclusion criteria.…”

Section: Discussionsupporting

confidence: 90%

Post-Stroke Depression: Prevalence, Associated Factors, and Relationship to Disability in a Tertiary Care Center in Sri Lanka

Thambirajah¹,

Senanayake

Gooneratne

et al. 2022

JNRP

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Background and Objectives The prevalence of stroke in urban Sri Lanka is estimated at 10.4 per 1000 and is expected to rise. Post-stroke depression (PSD) is an independent predictor of poor long-term outcomes. It leads to suboptimal rehabilitation, decreased quality of life, and increased mortality and is under-recognized. The main objectives of this study were to estimate the prevalence of depression in stroke, assess factors associated with PSD, and assess the relationship of PSD to disability. Materials and Methods A descriptive cross-sectional study was conducted at the Neurology and Medical Ward, National Hospital of Sri Lanka. Non-probability, consecutive sampling was used to collect data from patients with ischemic stroke admitted from January 2019 to January 2020. Patients with significant pre-existing depression, cognitive impairment, and language deficits were excluded. A structured, pre-tested interviewer-administered questionnaire was used to assess the prevalence and associated factors of PSD. Beck's Depression Inventory (BDI) was administered 3 months following the stroke to screen for depression. Modified Rankin Score (MRS) was used to assess disability on admission, discharge, and at 3 months. Results Eighty-one stroke patients were screened. The mean age was 66.6 years (±standard deviation [SD]: 12.5). Male:female ratio was 1.2:1. Depression at 3 months of follow-up was observed in 35.8% (95% confidence interval [CI]: 25.4–47.2%) of participants. Following bivariate analysis, large vessel stroke (p < 0.001), cortical stroke (p < 0.001), frontal lobe lesions (p < 0.001), history of past stroke (p = 0.014), and sexual dysfunction (p = 0.026) were associated with increased risk of PSD. The odds of a person with severe disability developing PSD was 7.9 times more than a person with a less severe disability at discharge from hospital and at 3 months of follow-up (odds ratio [OR] =7.9; 95% CI: 2.7–23.3, p = 0.000). Conclusions PSD occurs in one-third of strokes, keeping with previous studies. The risk of having PSD is higher among patients with severe disabilities. The difference in risk factors identified compared with previous studies can be attributable to differences in methodology. Identifying risk factors for post-stroke depression is essential to mitigate the poor outcome.

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Section: Discussionsupporting

confidence: 90%

Post-Stroke Depression: Prevalence, Associated Factors, and Relationship to Disability in a Tertiary Care Center in Sri Lanka

Thambirajah¹,

Senanayake

Gooneratne

et al. 2022

JNRP

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“…Despite the mechanisms of anxiety and depression are still unclear, neurotransmitters such as serotonin [also named 5-hydroxytryptamine (5-HT)], dopamine (DA), and noradrenaline (NE) have explained the pathophysiology of anxiety and depression over several decades ( Olivier and Olivier, 2020 ; Shao and Zhu, 2020 ). An increasing number of evidence reveals the importance of the gut microbiota in the pathogenesis of anxiety and depression ( Rieder et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

Brain Neurotransmitter Modulation by Gut Microbiota in Anxiety and Depression

Huang

2021

Front. Cell Dev. Biol.

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Anxiety and depression are highly prevalent mental illnesses worldwide and have long been thought to be closely associated to neurotransmitter modulation. There is growing evidence indicating that changes in the composition of the gut microbiota are related to mental health including anxiety and depression. In this review, we focus on combining the intestinal microbiota with serotonergic, dopaminergic, and noradrenergic neurotransmission in brain, with special emphasis on the anxiety- and depression-like behaviors in stress-related rodent models. Therefore, we reviewed studies conducted on germ-free rodents, or in animals subjected to microbiota absence using antibiotics, as well as via the usage of probiotics. All the results strongly support that the brain neurotransmitter modulation by gut microbiota is indispensable to the physiopathology of anxiety and depression. However, a lot of work is needed to determine how gut microbiota mediated neurotransmission in human brain has any physiological significance and, if any, how it can be used in therapy. Overall, the gut microbiota provides a novel way to alter neurotransmitter modulation in the brain and treat gut–brain axis diseases, such as anxiety and depression.

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“…Although much progress has been made in antidepressant treatment, nearly 80% of patients experience at least one recurrence in their lifetime ( 4 ). At present, the exact pathophysiological mechanism of depression is still elusive, various hypotheses have been proposed to explain this disease, including monoamine neurotransmitter disturbance, hypothalamic/pituitary/adrenal (HPA) axis disorder, neurotrophic factor deficiency, and immune dysfunction ( 5 , 6 ). Increasing evidence shows that classic antidepressants targeting serotonergic neurons may be ineffective in a considerable part of patients ( 7 ).…”

Section: Introductionmentioning

confidence: 99%

NLRP3/caspase-1/GSDMD–mediated pyroptosis exerts a crucial role in astrocyte pathological injury in mouse model of depression

Li¹,

Sun²,

Song³

et al. 2021

JCI Insight

135

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Emerging evidence suggests that astrocyte loss is one of the most important pathological features in the hippocampus of patients with major depressive disorder (MDD) and depressive mice. Pyroptosis is a recently discovered form of programmed cell death depending on Caspase–gasdermin D (Casp-GSDMD), which is involved in multiple neuropsychiatric diseases. However, the involvement of pyroptosis in the onset of MDD and glial pathological injury remains obscure. Here, we observed that depressive mice showed astrocytic pyroptosis, which was responsible for astrocyte loss, and selective serotonin reuptake inhibitor (SSRI) treatment could attenuate the pyroptosis induced by the chronic mild stress (CMS) model. Genetic KO of GSDMD, Casp-1, and astrocytic NOD-like receptor protein 3 (NLRP3) inflammasome in mice alleviated depression-like behaviors and inhibited the pyroptosis-associated protein expression. In contrast, overexpression of astrocytic GSDMD–N-terminal domain (GSDMD-N) in the hippocampus could abolish the improvement of behavioral alterations in GSDMD-deficient mice. This work illustrates that targeting the NLRP3/Casp-1/GSDMD–mediated pyroptosis may provide potential therapeutic benefits to stress-related astrocyte loss in the pathogenesis of depression.

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Associations Among Monoamine Neurotransmitter Pathways, Personality Traits, and Major Depressive Disorder

Cited by 47 publications

References 297 publications

Post-Stroke Depression: Prevalence, Associated Factors, and Relationship to Disability in a Tertiary Care Center in Sri Lanka

Post-Stroke Depression: Prevalence, Associated Factors, and Relationship to Disability in a Tertiary Care Center in Sri Lanka

Brain Neurotransmitter Modulation by Gut Microbiota in Anxiety and Depression

NLRP3/caspase-1/GSDMD–mediated pyroptosis exerts a crucial role in astrocyte pathological injury in mouse model of depression

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