Antidepressant Effect of Ketamine on Inflammation-Mediated Cytokine Dysregulation in Adults with Treatment-Resistant Depression: Rapid Systematic Review

Sukhram, Shiryn D.; Yilmaz, Grozdena; Gu, Jianying

doi:10.1155/2022/1061274

Cited by 9 publications

(5 citation statements)

References 57 publications

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“…Chronic stress is a major risk factor for MDD and has been associated with increased hypothalamic-pituitary-adrenal (HPA) axis activity and inflammatory activation of immune cells [7]. Increased levels of proinflammatory cytokines in the serum of depressed patients have inspired neuroscientists to investigate the possible role of neuroinflammation in depressive behavior [8]. This ushered in a new era in the neuropsychiatric field, leading to identifying brain immune cells, particularly microglia, as one of the prominent regulators of inflammation in the depressed brain.…”

Section: Introductionmentioning

confidence: 99%

Microglial Responses to Stress-Induced Depression: Causes and Consequences

Suk

2023

Cells

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Chronic stress is a major risk factor for various psychiatric diseases, including depression; it triggers various cellular and structural changes, resulting in the alteration of neurocircuitry and subsequent development of depression. Accumulating evidence suggests that microglial cells orchestrate stress-induced depression. Preclinical studies of stress-induced depression revealed microglial inflammatory activation in regions of the brain that regulate mood. Although studies have identified several molecules that trigger inflammatory responses in microglia, the pathways that regulate stress-induced microglial activation remain unclear. Understanding the exact triggers that induce microglial inflammatory activation can help find therapeutic targets in order to treat depression. In the current review, we summarize the recent literature on possible sources of microglial inflammatory activation in animal models of chronic stress-induced depression. In addition, we describe how microglial inflammatory signaling affects neuronal health and causes depressive-like behavior in animal models. Finally, we propose ways to target the microglial inflammatory cascade to treat depressive disorders.

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Section: Introductionmentioning

confidence: 99%

Microglial Responses to Stress-Induced Depression: Causes and Consequences

Suk

2023

Cells

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“…Ketamines have recently been used more frequently as they are thought to be more immediately effective than antidepressants. In a review entitled "Antidepressant effects of ketamines on inflammation-mediated serotonin dysregulation", ketamine infusions in 5 to 7 studies have notably decreased depression by 50% in 56% of those treated [65]. The effects reputedly involve a reduction in pro-inflammatory cytokines including IL-6 and TNF-1.…”

Section: Sleep Deprivation Shanafimentioning

confidence: 99%

Late Life Depression: A Narrative Review

2023

Int J Geriatr Gerontol

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The recent literature (last five years) on late life depression is predominantly focused on risk factors/predictors of late life depression along with studies on effects, buffers, and interventions. Late life depression has typically been self-reported or diagnosed starting at age 60. The prevalence rates for late life depression were highly variable in this literature, ranging from a low of 7% in Italy to a high of 37% in Chile, a variability that may relate to the year or type of data collection and/or crosscultural variation. Negative effects have included loneliness, suicidal ideation, cognitive decline, frailty, functional limitations, low heart rate variability, biological aging (short telomere length and white matter lesions) and earlier mortality. Risk factors have included loneliness, aging anxiety, life stressors (marital discord and job strain), physical problems (activities of daily living), physical health (elevated blood pressure), physical weakness (handgrip, frailty, falls and disability) and unhealthy intake (poor diet, excessive alcohol and vitamin D deficiency). Buffers/protective factors have included positive views on aging, resilience, practicing religion, a Mediterranean diet, and remaining active. Interventions have included cognitive training, mindfulness, physical activity and ketamines. Multiple underlying mechanisms have been suggested including dysfunctional connectivity between different networks in the brain. Although the data highlight the severity of late life depression, the recent literature has been based on different measures appearing on self-report surveys that have yielded mixed results across samples. Prevalence of Late Life DepressionFirst, some myths about late life depression in a paper entitled "Depression among older adults: A 2-year update on common myths and misconceptions" are worth summarizing [1]. These authors concluded: 1) depression is not more common in older adults; 2) late life depression is not more often caused by psychological factors; 3) those who experience late life depression respond to psychological interventions as well as younger adults, but not to antidepressants; 4) late life depression follows a more chronic course (i.e. a greater rate of relapse); and 5) late life depression is frequently moderated by comorbidity.

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“…Pharmacological studies have also confirmed the interconnection between depression and inflammation. Several antidepressants have been shown to reduce inflammation in both preclinical ( 11 ) and clinical ( 12 , 13 ) models of neuropsychiatric disorders. Antidepressants such as selective serotonin reuptake inhibitors fluoxetine ( 14 ) and paroxetine, tricyclic antidepressants amitriptyline and clomipramine, and monoamine oxidase inhibitors tranylcypromine can prevent LPS-induced microglial changes and the production of inflammatory markers interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) ( 15 ).…”

Section: Introductionmentioning

confidence: 99%

Lipopolysaccharide-induced depression-like model in mice: meta-analysis and systematic evaluation

Yin

Zhang

et al. 2023

Front. Immunol.

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Depression is a complex and biologically heterogeneous disorder. Recent studies have shown that central nervous system (CNS) inflammation plays a key role in the development of depression. Lipopolysaccharide (LPS)-induced depression-like model in mice is commonly used to studying the mechanisms of inflammation-associated depression and the therapeutic effects of drugs. Numerous LPS-induced depression-like models in mice exist and differ widely in animal characteristics and methodological parameters. Here, we systematically reviewed studies on PubMed from January 2017 to July 2022 and performed cardinal of 170 studies and meta-analyses of 61 studies to support finding suitable animal models for future experimental studies on inflammation-associated depression. Mouse strains, LPS administration, and behavioral outcomes of these models have been assessed. In the meta-analysis, forced swimming test (FST) was used to evaluate the effect size of different mouse strains and LPS doses. The results revealed large effect sizes in ICR and Swiss mice, but less heterogeneity in C57BL/6 mice. For LPS intraperitoneal dose, the difference did not affect behavioral outcomes in C57BL/6 mice. However, in ICR mice, the most significant effect on behavioral outcomes was observed after the injection of 0.5 mg/kg LPS. Our results suggests that mice strains and LPS administration play a key role in the evaluation of behavioral outcomes in such models.

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Antidepressant Effect of Ketamine on Inflammation-Mediated Cytokine Dysregulation in Adults with Treatment-Resistant Depression: Rapid Systematic Review

Cited by 9 publications

References 57 publications

Microglial Responses to Stress-Induced Depression: Causes and Consequences

Microglial Responses to Stress-Induced Depression: Causes and Consequences

Late Life Depression: A Narrative Review

Lipopolysaccharide-induced depression-like model in mice: meta-analysis and systematic evaluation

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