ABSTRACT
PURPOSE: Major Depressive Disorder (MDD) and Insomnia Disorder (ID) are prevalent psychiatric conditions often occurring concurrently, leading to substantial impairment in daily functioning. Understanding the neurobiological underpinnings of these disorders and their comorbidity is crucial for developing effective interventions. This study aims to analyze changes in functional connectivity within attention networks and default mode networks in patients with depression and insomnia. METHODS: The functional connectivity alterations in individuals with MDD, ID, comorbid MDD and insomnia (iMDD), and healthy controls (HC) were assessed from a cohort of 174 participants. They underwent rs-fMRI scans, demographic assessments, and scale evaluations for depression and sleep quality. Functional connectivity analysis was conducted using region-of-interest (ROI) and whole-brain methods. RESULTS: The MDD and iMDD groups exhibited higher Hamilton Depression Scale (HAMD) scores compared to HC and ID groups (P < 0.001). Both ID and MDD groups displayed enhanced connectivity between the left and right orbital frontal cortex compared to HC (P < 0.05), while the iMDD group showed reduced connectivity compared to HC and ID groups (P < 0.05). In the left insula, reduced connectivity with the right medial superior frontal gyrus was observed across patient groups compared to HC (P < 0.05), with the iMDD group showing increased connectivity compared to MDD (P < 0.05). Moreover, alterations in functional connectivity between the left thalamus and left temporal pole were found in iMDD compared to HC and MDD (P < 0.05). Correlation analyses revealed associations between abnormal connectivity and symptom severity in MDD and ID groups. CONCLUSIONS: Our findings demonstrate distinct patterns of altered functional connectivity in individuals with MDD, ID, and iMDD compared to healthy controls. These findings contribute to a better understanding of the pathophysiology of depression and insomnia, which could be used as a reference for the diagnosis and treatments of these patients.
Subject(s)
Default Mode Network , Depressive Disorder, Major , Magnetic Resonance Imaging , Sleep Initiation and Maintenance Disorders , Humans , Sleep Initiation and Maintenance Disorders/physiopathology , Sleep Initiation and Maintenance Disorders/diagnostic imaging , Male , Female , Adult , Depressive Disorder, Major/physiopathology , Middle Aged , Default Mode Network/physiopathology , Nerve Net/physiopathology , Nerve Net/diagnostic imaging , Attention/physiology , Comorbidity , Brain/physiopathology , Brain/diagnostic imaging , ConnectomeABSTRACT
Polygala tenuifolia Wild is an ancient traditional Chinese medicine. Its main component, tenuifolin (TEN), has been proven to improve cognitive impairment caused by neurodegenerative diseases and ovariectomy. However, there was hardly any pharmacological research about TEN and its potential gender differences. Considering the reduction of TEN on learning and memory dysfunction in ovariectomized animals, therefore, we focused on the impact of TEN in different mice genders in the current study. Spontaneous alternation behavior (SAB), light-dark discrimination, and Morris water maze (MWM) tests were used to evaluate the mice's learning and memory abilities. The field excitatory postsynaptic potential (fEPSP) of the hippocampal CA1 region was recorded using an electrophysiological method, and the morphology of the dendritic structure was examined using Golgi staining. In the behavioral experiments, TEN improved the correct rate in female mice in the SAB test, the correct rate in the light-dark discrimination test, and the number of crossing platforms in the MWM test. Additionally, TEN reduced the latency of female mice rather than male mice in light-dark discrimination and MWM tests. Moreover, TEN could significantly increase the slope of fEPSP in hippocampal Schaffer-CA1 and enhance the total length and the number of intersections of dendrites in the hippocampal CA1 area in female mice but not in male mice. Collectively, the results of the current study showed that TEN improved learning and memory by regulating long-term potentiation (LTP) and dendritic structure of hippocampal CA1 area in female mice but not in males. These findings would help to explore the improvement mechanism of TEN on cognition and expand the knowledge of the potential therapeutic value of TEN in the treatment of cognitive impairment.
Subject(s)
CA1 Region, Hippocampal , Dendrites , Diterpenes, Kaurane , Long-Term Potentiation , Animals , Female , Male , CA1 Region, Hippocampal/drug effects , Long-Term Potentiation/drug effects , Long-Term Potentiation/physiology , Mice , Dendrites/drug effects , Memory/drug effects , Sex Factors , Excitatory Postsynaptic Potentials/drug effects , Excitatory Postsynaptic Potentials/physiology , Maze Learning/drug effects , Maze Learning/physiologyABSTRACT
Whiteleg shrimp (Litopenaeus vannamei) is the most important species of shrimp farmed worldwide in terms of its economic value. Enterocytozoon hepatopenaei (EHP) infects the hepatopancreas, resulting in the hepatopancreatic microsporidiosis (HPM) of the host, which causes slow growth of the shrimp and poses a threat to the farming industry. In this study, differentially expressed proteins (DEPs) between EHP-infected and uninfected shrimp were investigated through proteomics sequencing. A total of 9908 peptides and 2092 proteins were identified. A total of 69 DEPs were identified in the hepatopancreas (HP), of which, 28 were upregulated and 41 were downregulated. Our results showed that the differences among the level of multiple proteins involved in the apoptosis were significant after the EHP infection, which indicated that the apoptosis pathway was activated in whiteleg shrimp. In addition, expression leve of caspase 3 gene were identified related to the EHP infection. Furthermore, predictions of spatial structure, analysis of phylogeny and chromosome-level linearity of the caspase 3 protein were performed as well. In conclusion, a relatively complete proteomic data set of hepatopancreas tissues in whiteleg shrimp were established in this study. Findings about genes involved in the apoptosis here will provide a further understanding of the molecular mechanism of EHP infection in the internal immunity of whiteleg shrimp.
Subject(s)
Enterocytozoon , Penaeidae , Animals , Caspase 3/genetics , Proteomics , Penaeidae/geneticsABSTRACT
BACKGROUND: Previous studies have shown that insomnia affects human prefrontal function and that there are specific patterns of brain activation to counteract sleep and improve cognition. However, the effects of insomnia on the prefrontal cortex of MDD (major depressive disorder) patients and the patterns of activation to counteract sleep in MDD patients remain unclear. The aim of this study is to examine this using fNIRS (functional near-infrared spectroscopy). METHODS: Eighty depressed patients and 44 healthy controls were recruited for this study. fNIRS was used to assess changes in the concentration of oxygenated hemoglobin ([oxy-Hb]) in the prefrontal cortex of all participants during the VFT (verbal fluency test) and to record the number of words created to assess cognitive ability. The Pittsburgh Sleep Quality Index was used to assess sleep quality, and the Hamilton Rating Scale for Depression (24-item) and Hamilton Rating Scale for Anxiety (14-item) were used to assess the severity of depression and anxiety. RESULTS: When comparing patients, the healthy control group had significantly higher [oxy-Hb] values in the bilateral prefrontal cortex during VFT than the MDD group. In the MDD group, the [oxy-Hb] values in all brain regions except the right DLPFC were significantly higher in the group with insomnia than in the group without insomnia, but their VFT performance was significantly lower than in the group without insomnia and the healthy group. PSQI scores were positively correlated with [oxy-Hb] values in some left-brain regions, whereas HAMD and HAMA scores were not correlated with [oxy-Hb] values. CONCLUSION: The PFC was significantly less active during VFT in those with MDD than in healthy controls. All brain regions, except the right DLPFC, were significantly more active in MDD patients with insomnia than in those without insomnia, suggesting that sleep quality needs to be an important indicator in fNIRS screening. In addition, there was a positive correlation between the severity of insomnia in the left VLPFC and the level of activation, suggesting a role for the left brain region in the neurophysiology of overcoming sleepiness in MDD patients. these findings may provide new ideas for the treatment of MDD patients in the future. TRIAL REGISTRATION: Our experiment was registered in the China Clinical Trial Registry (registration number ChiCTR2200065622) on November 10.( The first patient was recruited in 10/11/2022.).
Subject(s)
Depressive Disorder, Major , Sleep Initiation and Maintenance Disorders , Humans , Anxiety , Depression , Depressive Disorder, Major/diagnosis , Prefrontal Cortex/diagnostic imaging , Spectroscopy, Near-Infrared/methods , Sleep Initiation and Maintenance Disorders/complicationsABSTRACT
Objective: This paper aimed to probe changes in the default mode network (DMN) functional connectivity (DMNFC) of the brain of patients with insomnia disorder (ID) under the resting state. Methods: A total of 67 patients with ID and 67 graphically matched healthy controls were selected. Then, their general information was collected, followed by a psychological scale valuation. Resting state functional magnetic resonance imaging (rs-fMRI) scanning was conducted. Subsequently, collected statistics were processed, bilateral precuneus and medial superior frontal gyrus were defined as regions of interest (ROI), and the difference in intensity between these two groups was compared. Results: Compared with the healthy control group, the patients in the ID group were observed with abnormalities of DMNFC. Specifically, a significant increase in the functional connectivity (FC) could be observed between the left medial superior frontal gyrus and left central anterior gyrus, the left medial superior frontal gyrus and anterior cingulate gyrus, the right medial superior frontal gyrus and left central anterior gyrus, the left anterior cuneiform and left central anterior/posterior gyrus, the left anterior cuneiform and left superior occipital gyrus, as well as the right anterior cuneiform and left central posterior gyrus. However, the FC between the left anterior cuneiform and the right middle frontal gyrus was weakened, as well as between the left anterior cuneiform and the right angle gyrus and between the right precuneus and the left inferior temporal gyrus. Conclusion: ID patients may suffer changes in FC. The decline of FC in DMN may be one of the underlying causes of ID; the enhancement of FC between DMN and the visual-spatial attention network may play a key role in the mechanisms of impaired brain functional networks of ID.
Subject(s)
Brain Mapping , Sleep Initiation and Maintenance Disorders , Brain/diagnostic imaging , Brain Mapping/methods , Default Mode Network , Humans , Magnetic Resonance Imaging/methods , Sleep Initiation and Maintenance Disorders/diagnostic imagingABSTRACT
BACKGROUND: Recent studies suggest a correlation between the reduced Sirt-1 expression with Alzheimer's diseases (AD) and depression, respectively, suggesting a possible pathogenic role of the altered Sirt-1 expression in neuronal degenerative diseases, such as AD and depression. However, the molecular mechanisms underlying how Sirt-1 reduction impairs neuronal functions remain unknown. METHODS: We used the SK-N-SH neuroblastoma cells to study the role of Sirt-1 expression on physiological roles in neuronal cells. Gain of Sirt-1 was achieved by transiently transfecting Sirt-1 expression plasmid. Sirt-1-specific shRNA was used to elucidate the role of Sirt-1 loss of function. CCK-8 (Cell Counting Kit-8) assay and flow cytometry were used to evaluate cell proliferation. Semiquantitative western blotting was used to detect relative protein levels. A further luciferase reporter gene assay was employed to examine the effect of Sirt-1 expression on the transcriptional activity of p53. RT-qPCR was used to determine the mRNA levels of p21, Bax, and Bcl-2, which were the downstream target genes of p53. RESULTS: Sirt-1 suppressed the p53 downstream gene p21 transcription, while shRNA-mediated Sirt-1 knockdown resulted in a significant increase in p21 expression, implying a possibility that Sirt-1 promotes neuron proliferation through suppressing p53 transcriptional activity. The mRNA and protein levels of p53 were not affected by the altered Sirt-1 expression, suggesting that Sirt-1 regulates the transcriptional regulatory activity of p53 rather than p53 expression. Indeed, we further confirmed that Sirt-1 appeared to inhibit p53 transcriptional activity by attenuating its acetylation and resulted in a decrease of p53's binding to the p21 promoter. Overexpressed Sirt-1 scavenged reactive oxygen species (ROS) production in SK-N-SH with H2O2. Knockdown of Sirt-1 presented opposite effect; the addition of EX527 (Sirt-1 inhibitor) increased ROS accumulation. CONCLUSIONS: Oxidative stress induces Sirt-1 in neuron cells, and Sirt-1 promotes proliferation in SK-N-SH cells, which protects them from oxidative stress-induced cell death, potentially via suppressing the transcriptional activity of p53. These results provide a molecular explanation underlying how the reduced Sirt-1 potentially causes the AD and depression-related diseases, supporting the idea that Sirt-1 can possibly be used as a diagnostic biomarker and/or therapeutic drug target for the AD and depression-related diseases.
Subject(s)
Oxidative Stress , Protective Agents/metabolism , Sirtuin 1/metabolism , Acetylation/drug effects , Cell Line , Cell Movement/drug effects , Cell Proliferation/drug effects , Cyclin-Dependent Kinase Inhibitor p21/metabolism , Humans , Hydrogen Peroxide/toxicity , Lysine/metabolism , Neural Stem Cells/drug effects , Neural Stem Cells/metabolism , Neural Stem Cells/pathology , Neurons/drug effects , Neurons/metabolism , Neurons/pathology , Oxidative Stress/drug effects , Promoter Regions, Genetic/genetics , Protein Binding/drug effects , Reactive Oxygen Species/metabolism , Signal Transduction/drug effects , Transcription, Genetic/drug effects , Tumor Suppressor Protein p53/genetics , Tumor Suppressor Protein p53/metabolismABSTRACT
In this paper, we determined and characterized the complete mitochondrial genome of Pronghorn spiny lobster Panulirus penicillatus for the first time from South China Sea. The P. penicillatus mitogenome is 15,671 bp long, and consists of 22 tRNA genes, 2 rRNA genes, 13 protein-coding genes (PCGs), and 1 control region. The nucleotide composition of P. penicillatus mitogenome is significantly biased (A, G, T, and C was 33.62, 13.32, 32.31, and 20.75%, respectively) with A + T contents of 65.93%. Almost PCGs used a standard initiation codon or stop codon, except COX2, ND3, ND4 and ND1 were terminated with an incomplete stop codon T and ND5 ended with TA. One microsatellite (C)12 was identified in the control region of P. penicillatus mitogenome sequences. Phylogenetic tree showed that P. penicillatus was first clustered with P. polyphagus and P. versicolor.
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The complete mitochondrial genome of Trachycardium flavum from South China Sea was first determined in this study, which is 16,596 bp in length. The base composition of the mitogenome is a less biased (A, G, T, and C was 21.5%, 26.3%, 37.0%, and 15.2%, respectively) with A + T contents of 58%. It consists of 24 tRNA genes, two rRNA genes, and 12 protein-coding genes (PCGs). No typical control region was found in non-coding sequence. Interestingly, ATP8 genes was absence same as most shellfish. Nine PCGs use a special start codon TTG, and the other three genes use a normal initiation codon ATN. Except ND6 use a single base G as the stop codon, the others all end with the normal stop codon TAG. The phylogenetic tree showed that T. flavum was first clustered with Fulvia mutica, Cerastoderma edule, and Acanthocardia tuberculate, which all belong to Cardiidae.
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The complete mitochondrial genome of Anadara antiquata was first determined. With a length of 45,454 bp, it consists of 29 tRNA, 2 rRNA, and 17 protein-coding genes (PCGs). The non-coding region was large and atypical around the genome with total 24,162 bp long. The nucleotide composition is significantly biased with AT contents of 62.2%. PCGs have five types of start codon, and terminate with a complete stop codon TAA or TAG. 19 microsatellites (SSRs) were identified in mitogenome sequences. Phylogenetic analysis demonstrated that A. antiquata was first clustered with Anadara vellicate, then together with Tegillarca granosa.
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The complete mitochondrial genome of Cypraea tigris from the South China Sea has been determined, which was the first report of complete mitogenome in the superfamily Cypraeoidea. It is 16,177 bp long and consists of 21 tRNA genes, 2 rRNA genes, 13 protein-coding genes (PCGs), and 1 control region. The base composition of C. tigris mitogenome is biased (A, G, T, and C were 28.8, 17.9, 37.1, and 16.3%, respectively) with A + T contents of 58.5%. All of the PCGs use a typical start codon (ATN) and a complete stop codon (TAA or TAG) as normal. The maximum-likelihood tree demonstrated that the Cypraeoidea was closer to the superfamily Tonnoidea, and further clarified the phylogenetic relationships of each superfamily in Littorinimorpha.