Micro non-coding RNA (microRNA, miRNA) is a small non-coding RNA involved in gene expression regulation that plays an important role in the onset and development of mental illness. Evidence suggests that several miRNAs are dysregulated in patients with mental illnesses. Because of its stability and quantitative detection in peripheral blood and cerebral fluid, miRNA is a particularly attractive biomarker. The objective of this research is to investigate the relationship between mental illness and miRNAs, as well as the potential processes through which miRNAs contribute to disease etiology. Schizophrenia, bipolar disorder, and depression are three major mental disorders with high disability and mortality. The study explored the particular dysregulated miRNAs for each condition as well as common dysregulated miRNAs across diseases. In this study, which analyzes the findings from relevant studies from 2016 to 2020, the authors discuss the functions of numerous severely dysfunctional miRNAs and their application potential in the field of psychiatry research.
Biomarkers ; Bipolar Disorder/genetics* ; Depression/genetics* ; Humans ; MicroRNAs ; Schizophrenia/genetics*

OBJECTIVETo investigate the association between anxiety-depression and 5-HTTLPR gene polymorphism in school-aged twins.

METHODSA total of 147 pairs of twins (47 pairs of monozygotic twins, 100 pairs of dizygotic twins) aged 8-12 years from Baotou and Hohhot were selected as respondents. The Achenbach Child Behavior Checklist (CBCL) was used to calculate the scores of anxiety-depression factors in school-aged twins. The DNA was extracted from oral epithelial cells, and polymerase chain reaction was applied for 5-HTTLPR genotyping. The generalized estimating equation (GEE) was used to analyze the effect of 5-HTTLPR polymorphism and family environment on anxiety-depression in school-aged twins.

RESULTSThe children with LS and SS genotypes had significantly higher scores of anxiety-depression factors than those with LL genotype (χ2=3.938, P<0.05). The interaction of 5-HTTLPR genotype with family cohesion and family rearing patterns had a significant impact on the scores of anxiety-depression factors in twins (χ2=6.129 and 7.665, both P<0.05).

CONCLUSIONS5-HTTLPR genotype is significantly correlated with the scores of anxiety-depression factors in school-aged twins. In the family with high cohesion and an autocratic family rearing pattern, S allele may increase the possibility of anxiety-depression in twin children.

Anxiety ; genetics ; Child ; Depression ; genetics ; Female ; Genotype ; Humans ; Male ; Polymorphism, Genetic ; Serotonin Plasma Membrane Transport Proteins ; genetics ; Twins ; genetics

OBJECTIVE: To investigate the differential expression of miR-30a-5p in patients with poststroke depression and explore the possible mechanism. METHODS: We obtained the target microRNAs through searching PubMed using the online software VENNY2.1. We collected the baseline demographic, clinical and radiographic data from consecutive patients with first-ever acute ischemic stroke on admission in our department from October, 2018 to March, 2019. From each patient, 5 mL peripheral venous blood was collected upon admission. Hamilton Depression Scale (HAMD-17) was used to evaluate the degree of depression at the end of the 3-month follow-up. The patients with a HAMD-17 score≥7 were diagnosed to have depression according to the diagnostic criteria of the Fourth Edition of the Diagnostic and Statistical Manual of Mental Disorders of the American Psychiatric Association (DSM-IV). The patients were divided into post-stroke depression group (PSD group, =11) and non-post-stroke depression group (non-PSD group, =25), and their plasma levels of miR-30a-5p were detected using qPCR. The STARBASE Database ENCORI miRNA-mRNA module and Comparative Toxicogenomics Database were used to predict and screen the possible target genes related to miR-30a-5p, and the possible mechanism of the target genes was further analyzed through bioinformatics. RESULTS: miR-30a-5p was identified by cross-screening as the target miRNA associated with stroke and depression and showed obvious differential expression between PSD and non-PSD patients (2.462±0.326 1±0.126, < 0.0001). ROC curve analysis showed that the AUC of miR-30a-5p for predicting PSD was 0.869 (95%: 0.745-0.993, =0.0005) at the cutoff value of 1.597, with a sensitivity and specificity of 0.727 and 0.840, respectively. The target proteins of miR-30a-5p involved a wide range of biological processes, including signal transduction, intercellular communication, regulation of nucleobase, nucleoside, nucleotide and nucleic acid metabolism. KEGG pathway enrichment analysis showed that the target proteins affected mainly the neural nutrient signaling pathway, axon guidance signaling pathway and insulin signaling system. We also identified the top 20 HUB genes that might be associated with post-stroke depression. CONCLUSIONS Plasma miR-30a-5p is differentially expressed in PSD and can serve as a new blood marker for diagnosis and also a therapeutic target of PSD.
Brain Ischemia ; Computational Biology ; Depression ; etiology ; genetics ; Gene Expression Regulation, Neoplastic ; Humans ; MicroRNAs ; genetics ; Stroke ; complications

This study aimed to investigate the intervention effect and mechanism of Xiaoyao Kangai Jieyu Recipe(XKJR) on hip-pocampal microglia and neuronal damage in mice with breast cancer related depression. The mouse model of breast cancer related depression was established by inoculation of 4T1 breast cancer cells in axilla and subcutaneous injection of corticosterone(30 mg·kg~(-1)). The successfully modeled mice were randomly divided into a model group, a positive drug group(capecitabine 60 mg·kg~(-1)+fluoxetine 19.5 mg·kg~(-1)), and XKJR group(19.5 mg·kg~(-1) crude drug), with 6 in each group. Another 6 normal mice were taken as a normal group. The administration groups were given corresponding drugs by gavage, while the normal and model groups were given an equal volume of distilled water, once a day for 21 consecutive days. The depressive behavior of mice was assessed by glucose consumption test, open field test and novelty-suppressed feeding test. Hematoxylin and eosin(HE) staining and tumor suppression rate were used to evaluate the changes of axillary tumors. The mRNA expressions and the relative protein expressions of interleukin-1β(IL-1β), interleukin-18(IL-18), cyclooxyganese-2(COX-2) and glutamyl-prolyl-tRNA synthetase(EPRs) in the hippocampus of mice were determined by quantitative real-time polymerase chain reaction(qRT-PCR) and immunohistochemistry, respectively. Immunofluorescence was performed to detect the mean fluorescence intensity of CD11b, a marker of hippocampal microglia activation. Nissler staining and transmission electron microscopy were employed to observe the morphological changes and the ultramorphological changes of hippocampal neurons, respectively. The experimental results indicated that compared with the normal group, the model group had reduced glucose consumption and lowered number of total activities in open field test(P<0.05, P<0.01), prolonged first feeding latency in no-velty-suppressed feeding test(P<0.01), and significant depression-like behavior; the contents of IL-1β, IL-18, COX-2, and EPRs in hippocampus were increased(P<0.05, P<0.01), with hippocampal microglia activation and obvious neuronal damage. Compared with the model group, the positive drug group and the XKJR group presented an improvement in depressive behaviors, a decrease in the contents of IL-1β, IL-18, COX-2 and EPRs in hippocampus, and an alleviation in the activation of hippocampal microglia and neuronal damage; the tumor suppression rates of positive drug and XKJR were 40.32% and 48.83%, respectively, suggesting a lower tumor growth rate than that of the model group. In summary, XKJR may improve hippocampal microglia activation and neuronal damage in mice with breast cancer related depression through activating COX signaling pathway.
Mice ; Animals ; Depression/genetics* ; Interleukin-18 ; Cyclooxygenase 2/genetics* ; Hippocampus ; Glucose ; Neoplasms

P-glycoprotein (P-gp) is encoded by the ABCB1 gene and acts as an efflux pump for xenobiotics. In the Border Collie, a nonsense mutation caused by a 4-base pair deletion in the ABCB1 gene is associated with a premature stop to P-gp synthesis. In this study, we examined the full-length coding sequence of the ABCB1 gene in an ivermectin-sensitive Border Collie that lacked the aforementioned deletion mutation. The sequence was compared to the corresponding sequences of a wild-type Beagle and seven ivermectin-tolerant family members of the Border Collie. When compared to the wild-type Beagle sequence, that of the ivermectin-sensitive Border Collie was found to have one insertion mutation and eight single nucleotide polymorphisms (SNPs) in the coding sequence of the ABCB1 gene. While the eight SNPs were also found in the family members' sequences, the insertion mutation was found only in the ivermectin-sensitive dog. These results suggest the possibility that the SNPs are species-specific features of the ABCB1 gene in Border Collies, and that the insertion mutation may be related to ivermectin intolerance.
ATP-Binding Cassette Transporters/*genetics ; Animals ; Depression/chemically induced ; Dogs/*genetics ; Female ; Ivermectin/*adverse effects ; Male ; Mutagenesis, Insertional/*genetics ; Polymorphism, Single Nucleotide/genetics ; Sialorrhea/chemically induced

This article reviews the recent literature of 'vascular depression' hypothesis. The 'vascular depression' hypothesis is supported by the evidence for associations between vascular disease and late-onset depression and between ischemic brain lesions and distinctive depressive symptoms. Patients with vascular depression is characterized by late-onset, absence of family history of mood disorders, evidence of vascular disease or vascular risk factors, cognitive impairment, psychomotor retardation, limited depressive ideation, poor insight, and disability. Vascular depression may be the entity suitable for studies of mechanism of depression. Depression in later life is often under-diagnosed and under-treated. Drugs used in the prevention and treatment of cerebrovascular disease may be shown to be beneficial influences for the prevention of vascular depression. Combined treatment with antidepressant and cognitive-behavioral rehabilitation will be more helpful. In the future, developments in structural and functional imaging, electrophysiology, chronobiology, and genetics will permit the knowledge of the association between mood disorders and brain lesions.
Brain ; Depression* ; Electrophysiology ; Genetics ; Humans ; Mood Disorders ; Psychomotor Disorders ; Rehabilitation ; Risk Factors ; Vascular Diseases

As a kind of mental illness, depression produces great difficulties in clinical diagnosis and treatment, and has a high disability rate. It is urgent to clarify the mechanism of depression to find potential therapeutic targets and effective clinical treatment methods. As a deacetylase, silent mating type information regulator 2 homolog 1 (SIRT1) is involved in many biological processes such as cell aging, cancer, and cardiovascular disease. In recent years, more and more studies have found that SIRT1 gene plays an important role in the pathogenesis of depression, but the mechanism is still unclear. Therefore, this review mainly summarizes the relevant research progress on the role and mechanism of SIRT1 gene in the hippocampus, prefrontal cortex, amygdala, hypothalamic suprachiasmatic nucleus, and nucleus accumbens in depression, in order to provide new ideas for exploring the mechanism and prevention of depression.
Cellular Senescence ; Depression/genetics* ; Hippocampus/metabolism* ; Humans ; Nucleus Accumbens ; Sirtuin 1/metabolism*

The important role that gonadal hormones play in women's life is also manifested in regulation of mood and behavior. Estrogen, in particular, has mostly positive effects on women's mood, while some periods of hormonal change like the postpartum, perimenstrual period and the perimenopause are associated with increased risk of depression. The propensity of women to develop depression seems to be due to a combined effect of genetics, gonadal hormones, and psychosocial factors. The sex difference of neuroanatomical response to mood, and changes in modulation of monoamine neurotransmitters by gonadal hormones, also seemed to be a risk factor to increase the vulnerability to depression in women.
Depression* ; Depression, Postpartum ; Estrogens ; Female ; Genetics ; Gonadal Hormones ; Humans ; Limbic System ; Neurobiology* ; Neurotransmitter Agents ; Perimenopause ; Postpartum Period ; Psychology ; Risk Factors ; Serotonin ; Sex Characteristics

OBJECTIVETo explore the molecular genetic mechanism of complicating depression in asthma by detecting two gene polymorphisms of 5-hydroxytryptamine transporter (5-HTTLPR/Stin2) gene.

METHODSOne hundred fifty-six adults with asthma were collected, and divided into group of asthma with depression (HAMD score > or = 8) and group of asthma without depression or single asthma (HAMD score <8) according to the score of Hamilton depression scale (HAMD). A total of 508 adults with depression alone and 433 healthy individuals were enrolled as controls. The target gene fragments containing the polymorphic regions of 5-HTTLPR and Stin2 were amplified by polymerase chain reaction (PCR). The amplified fragments were then analyzed using agarose gel electrophoresis (AGE) and motored molecular imaging system.

RESULTSThe frequencies of genotype and allele distribution of the Stin2 polymorphism showed that males with genotype Stin2.12/Stin2.10 and allele Stin2.10 had higher risk for asthma than the others (Stin2.12/Stin2.10: OR = 2.291, 95% CI: 1.195 and 4.390; Stin2.10: OR = 1.942, 95% CI: 1.069-3.527). No significant difference was found in the frequencies of genotype and allele distribution of the 5-HTTLPR locus between the asthma and healthy control groups and the two stratified by gender.

CONCLUSIONThe Stin2 polymorphism may play a role in the onset of male asthma. There might be association between the genetic pathogenesis of asthma and depression.

Adult ; Alleles ; Asthma ; epidemiology ; genetics ; Case-Control Studies ; Comorbidity ; Depression ; epidemiology ; genetics ; Female ; Genome-Wide Association Study ; Genotype ; Humans ; Male ; Polymorphism, Genetic ; Serotonin Plasma Membrane Transport Proteins ; genetics

OBJECTIVETo explore the possible mechanism(s) of taurine-inhibiting the proliferation of hepatic stellate cells (HSC), this study investigated the effect of taurine on the HSC cell cycle and its regulatory protein expression.

METHODSCell proliferation was assessed by MTT assay. Cell cycle was analyzed by flow cytometry. Cell cycle regulatory protein Cyclin D1 and P21waf1 expression were determined by immunocytochemistry and image-analysis system, and real-time quantitative PCR.

RESULTSHSC proliferation was markedly inhibited when HSC were treated with taurine at concentrations of 5, 10, 20, 30, 40 and 50 mmol/L for 48 hours, and the inhibition rates were 6.7%, 14.4%, 23.3%, 32.2%, 36.7% and 45.6% respectively (P < 0.05-0.01). In the flow cytometry analysis, it was found that taurine could block HSC in the G0/G1 phase from entering the S phase, resulting in more cells in the G0/G1 phase and fewer in the S phase. The percentage of the cells in the G0/G1 phase and the S phase at the dosage of 40 mmol/L were 68.2%+/-1.4% and 26.2+/-1.3% respectively, which was significantly different in comparison to the controls (56.2%+/-1.7% and 38.5%+/-0.8% respectively, P < 0.01). HSC expressed cyclin D1 and P21waf1. Taurine inhibited cyclin D1 expression and induced P21waf1 expression. The cyclin D1 protein and mRNA in the HSC treated with 40 mmol/L taurine were significantly reduced compared with the controls [protein (optical density value): 0.13+/-0.02 versus 0.18+/-0.02, P < 0.01; mRNA: 5776.7+/-3345.0 versus 18,400.6+/-1374.8 copies/10(6) GAPDH, P < 0.01]; and the P21waf1 protein and mRNA were markedly increased compared with the controls [protein (optical density value): 0.19+/-0.02 versus 0.14+/-0.01, P < 0.01; mRNA: 44,866.7+/-3910.7 versus 16,933.3+/-960.9 copies/10(6) GAPDH, P less than 0.05].

CONCLUSIONSCyclin D1 and P21waf1 were cell cycle regulatory proteins in HSC, and taurine can inhibit the HSC cyclin D1 expression and stimulate P21waf1 expression, facilitate arresting cells in G0/G1 phase, and suppress cell proliferation.

Animals ; Cell Cycle Proteins ; biosynthesis ; genetics ; Cell Line ; Cell Proliferation ; Cyclin D1 ; biosynthesis ; genetics ; Cyclin-Dependent Kinase Inhibitor p21 ; biosynthesis ; genetics ; Depression, Chemical ; Hepatocytes ; cytology ; Rats ; Taurine ; pharmacology