Serum-based microRNA biomarkers for major depression: MiR-16, miR-135a, and miR-1202

Gheysarzadeh, Ali; Sadeghifard, Nourkhoda; Afraidooni, Loghman; Pooyan, Farahnaz; Mofid, Mohammad Reza; Valadbeigi, Hassan; Bakhtiari, Hadi; Keikhavani, Sattar

doi:10.4103/jrms.jrms_879_17

Cited by 63 publications

(43 citation statements)

References 29 publications

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“…One study indicated that serum levels of miRNA-16 are increased in rats after CUMS [60]. In contrast, clinical reports revealed that serum levels of miRNA-16 are reduced in patients with depression [43]. In the present study, we found the disease model caused overall upregulated miRNA-16 levels in the hippocampus but did not significantly affect serum miRNA-16 levels.…”

contrasting

confidence: 67%

“…However, few studies have focused on serum levels of miRNA-16 in patients with depression. A recent study reported that the level of serum miRNA-16 was significantly decreased in patients with depression, which suggests that miRNA-16 has potential as a high-specificity and highsensitivity biomarker for depression [43]. e present study aimed to answer the following question: what is the relationship between miRNA-16 and 5-HT in the hippocampus and serum?…”

Section: Introductionmentioning

confidence: 91%

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Effect of Electroacupuncture on Reuptake of Serotonin via miRNA-16 Expression in a Rat Model of Depression

Zhao

Tian

Song

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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The current study aimed to investigate the effects and mechanisms of electroacupuncture (EA) treatment applied to Bai hui (GV20) and Yin tang (GV29) acupoints (1 mA, 2 Hz, continuous wave, 20 minutes) for 28 days in a rat model of chronic unpredictable mild stress (CUMS) on reuptake of serotonin (5-hydroxytryptamine (5-HT)) and miRNA-16 levels in the hippocampus and serum. Rats were housed in individual cages, and CUMS was used to establish a rat model of depression. After EA treatment for 4 weeks, behavioral changes and indices including 5-HT transporter (SERT), 5-HT, and miRNA-16 levels in the hippocampus and serum were examined. The EA treatment significantly improved base levels of sucrose preference and exploratory behavior and significantly decreased SERT protein and mRNA expression in the hippocampus of depressed rats. Significantly increased 5-HT levels were observed, and miRNA-16 levels were significantly decreased in the hippocampus and serum of depressed rats. In conclusion, the antidepressant effects of EA treatment may be affected via inhibition of 5-HT reuptake, upregulation of 5-HT levels, and inhibition of miRNA-16 expression in the hippocampus and serum.

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contrasting

confidence: 67%

Section: Introductionmentioning

confidence: 91%

Effect of Electroacupuncture on Reuptake of Serotonin via miRNA-16 Expression in a Rat Model of Depression

Zhao

Tian

Song

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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“…ID J:208678). Both the miRs are decreased in the blood of MDD patients [120], which corresponds to an increased level of GSK3β [39]. Moreover, miR16 regulates the expression of 5-HT transporter (SERT) [121], while miR135a is associated with the regulation of the expression of SERT and 5-HT 1A R [122].…”

Section: β-Catenin Destruction Complexmentioning

confidence: 99%

GSK3β: A Master Player in Depressive Disorder Pathogenesis and Treatment Responsiveness

Duda

Hajka

Wójcicka

et al. 2020

Cells

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Glycogen synthase kinase 3β (GSK3β), originally described as a negative regulator of glycogen synthesis, is a molecular hub linking numerous signaling pathways in a cell. Specific GSK3β inhibitors have anti-depressant effects and reduce depressive-like behavior in animal models of depression. Therefore, GSK3β is suggested to be engaged in the pathogenesis of major depressive disorder, and to be a target and/or modifier of anti-depressants' action. In this review, we discuss abnormalities in the activity of GSK3β and its upstream regulators in different brain regions during depressive episodes. Additionally, putative role(s) of GSK3β in the pathogenesis of depression and the influence of anti-depressants on GSK3β activity are discussed.Cells 2020, 9, 727 2 of 26 any of the groups listed above. Additionally, electroconvulsive therapy, conducted for the first time in 1938, is still widely used in the treatment of MDD, especially in its drug-refractory form [5].Although the monoaminergic hypothesis has led to the invention of many successful therapeutic strategies based on the elevation of levels of NA and 5-HT in the synaptic cleft, it does not explain the anti-depressant effect of lithium and the rapid action of ketamine in the treatment of mood disorders [6]. Therefore, factors other than neurotransmission must be taken into consideration in the context of the MDD pathogenesis. One of them is glycogen synthase kinase 3β (GSK3β) signaling. Glycogen Synthase Kinase 3βGSK3 was isolated in 1980, from rabbit skeletal muscle, and described as a highly specific serine/threonine kinase for glycogen synthase [7]. There are two isozymes of GSK3, α and β, and both are expressed at similar levels in the mouse brain [8]. In the human brain, the β isozyme predominates [9]. Therefore, GSK3β is expected to be crucial for the human central nervous system functioning. The activity of GSK3β is regulated positively and negatively by phosphorylation on Tyr216 and Ser9, respectively [10,11]. Whereas phosphorylation of the residue Tyr216 occurs during the GSK3β translation process and results in a synthesis of the fully activated kinase, Ser9 phosphorylation seems to be the main regulatory modification during the enzyme lifespan [12]. Ser9-phosphorylated GSK3β remains inhibited, and dephosphorylation of the residue results in the disinhibition (activation) of the kinase.GSK3β is part of numerous cellular signaling pathways, and its activity can be regulated, directly or indirectly, by several kinases, phosphatases, and proteases. The wide spectrum of GSK3β substrates, including transcription factors, glycolytic enzymes, pro-and anti-apoptotic factors, mitochondrial channels, membrane receptors, and cytoskeleton-associated proteins, makes GSK3β a central point of the cell homeostasis maintenance [13]. The activity of GSK3β affects energy metabolism, cell survival, proliferation, apoptosis, membrane polarity, internalization of the synaptic receptors, neuroplasticity, neurotransmission, amyloid processing, and many other processes [13].Ex...

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“…Much effort has been devoted to developing effective therapeutic agents. Recently, targeting microRNAs (miRNAs) with small molecules has become a novel therapy for human diseases (Gheysarzadeh et al, 2018). In other research, Meng et al, present a systematic computational approach to construct a bioactive Small molecule and miRNA association Network in AD (SmiRN-AD), which is based on the gene expression signatures of bioactive small molecule perturbation and AD-related miRNA regulation.…”

Section: Other Ad Treatment Productsmentioning

confidence: 99%

The recent development in synthesis and pharmacological evaluation of small molecule to treat Alzheimer's diseases: A review

2020

Int. J. Adv. Biol. Biomed. Res.

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Alzheimer's disease is a neurological disorder in which the death of brain cells causes memory loss and cognitive decline. It is a neurodegenerative type of dementia, the disease starts mild and gets progressively worse. Like all types of dementia, Alzheimer's is caused by brain cell death. The most common presentation marking Alzheimer's dementia is where symptoms of memory loss are the most prominent, especially in the area of learning and recalling new information. Alzheimer's disease is not simple to diagnose for which there is no single test. For this reason, the first thing doctors do is to rule out other problems before confirming whether mental signs and symptoms are severe enough to be a kind of dementia or something else. Genetic test is possible in some settings to indicate the likelihood of someone having or developing the disease but this is controversial and not entirely reliable. There are no disease-modifying drugs available for Alzheimer's disease but some options may reduce its symptoms and help improve quality of life. A different kind of drug, namely memantine, an NMDA receptor antagonist, may also be used, alone or in combination with a cholinesterase inhibitor. This review highlights the several reports that attempt to design and synthesis of some classes of selective Alzheimer's disease inhibitors.

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Serum-based microRNA biomarkers for major depression: MiR-16, miR-135a, and miR-1202

Cited by 63 publications

References 29 publications

Effect of Electroacupuncture on Reuptake of Serotonin via miRNA-16 Expression in a Rat Model of Depression

Effect of Electroacupuncture on Reuptake of Serotonin via miRNA-16 Expression in a Rat Model of Depression

GSK3β: A Master Player in Depressive Disorder Pathogenesis and Treatment Responsiveness

The recent development in synthesis and pharmacological evaluation of small molecule to treat Alzheimer's diseases: A review

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