Peripheral mitochondrial DNA as a neuroinflammatory biomarker for major depressive disorder

In the pathogenesis of major depressive disorder, chronic stress-related neuroinflammation hinders favorable prognosis and antidepressant response. Mitochondrial DNA may be an inflammatory trigger, after its release from stress-induced dysfunctional central nervous system mitochondria into peripheral circulation. This evidence supports the potential use of peripheral mitochondrial DNA as a neuroinflammatory biomarker for the diagnosis and treatment of major depressive disorder. Herein, we critically review the neuroinflammation theory in major depressive disorder, providing compelling evidence that mitochondrial DNA release acts as a critical biological substrate, and that it constitutes the neuroinflammatory disease pathway. After its release, mitochondrial DNA can be carried in the exosomes and transported to extracellular spaces in the central nervous system and peripheral circulation. Detectable exosomes render encaged mitochondrial DNA relatively stable. This mitochondrial DNA in peripheral circulation can thus be directly detected in clinical practice. These characteristics illustrate the potential for mitochondrial DNA to serve as an innovative clinical biomarker and molecular treatment target for major depressive disorder. This review also highlights the future potential value of clinical applications combining mitochondrial DNA with a panel of other biomarkers, to improve diagnostic precision in major depressive disorder.

Sleep disturbances and psychomotor retardation in the prediction of cognitive impairments in patients with major depressive disorder

BACKGROUND Symptoms of depression and comorbid anxiety are known risk factors for cognitive impairment in major depressive disorder(MDD).Understanding their relationships is crucial for developing targeted interventions to mitigate cognitive impairments in MDD patients.We expect that the severity of sleep disturbances and other depressive symptoms will be positively correlated with the degree of cognitive impairments.We also hypothesize that anxiety symptoms,especially psychic anxiety,is a key factor in predicting cognitive performance in MDD patients and may indirectly contribute to cognitive impairment by affecting sleep disturbances and other potential factors.AIM To determine which dimension of the depressive and anxiety symptoms predicts cognitive impairment during a depressive episode.METHODS A comprehensive neurocognitive test battery assessed executive function,attention,processing speed,and memory in 162 medication-free MDD patients and 142 matched healthy controls.The 24-item Hamilton Depression Rating Scale was used to assess depressive symptoms,and the 14-item Hamilton Anxiety Scale was used to assess anxiety symptoms.Linear regression analyses and mediation analyses were conducted to evaluate the impact of depressive and anxiety symptoms,as well as their interactions,on cognitive impairments.RESULTS Among the depressive symptoms,sleep disturbances were associated with poorer executive function(P=0.004),lower processing speed(P=0.047),and memory impairments(P<0.001),and psychomotor retardation(PR)was associated with lower processing speed in patients with MDD(P=0.019).Notably,PR was found to mediate the impact of sleep disturbances on the processing speed.Regarding anxiety symptoms,psychic anxiety,rather than somatic anxiety,was associated with cognitive impairments in all aspects.Sleep disturbances mediated the effect of psychic anxiety on executive function[β=-0.013,BC CI(-0.027,-0.001)]and memory[β=-0.149,BC CI(-0.237,-0.063)],while PR mediated its effect on processing speed(β=-0.023,BC CI(-0.045,-0.004)].CONCLUSION Sleep disturbances may be a key predictor of poorer executive function,lower processing speed,and memory loss,while PR is crucial for lower processing speed during a depressive episode.Psychic anxiety contributes to all aspects of cognitive impairments,mediated by sleep disturbances and PR.

Vulnerable brain regions in adolescent major depressive disorder:A resting-state functional magnetic resonance imaging activation likelihood estimation meta-analysis

BACKGROUND Adolescent major depressive disorder(MDD)is a significant mental health concern that often leads to recurrent depression in adulthood.Resting-state functional magnetic resonance imaging(rs-fMRI)offers unique insights into the neural mechanisms underlying this condition.However,despite previous research,the specific vulnerable brain regions affected in adolescent MDD patients have not been fully elucidated.AIM To identify consistent vulnerable brain regions in adolescent MDD patients using rs-fMRI and activation likelihood estimation(ALE)meta-analysis.METHODS We performed a comprehensive literature search through July 12,2023,for studies investigating brain functional changes in adolescent MDD patients.We utilized regional homogeneity(ReHo),amplitude of low-frequency fluctuations(ALFF)and fractional ALFF(fALFF)analyses.We compared the regions of aberrant spontaneous neural activity in adolescents with MDD vs healthy controls(HCs)using ALE.RESULTS Ten studies(369 adolescent MDD patients and 313 HCs)were included.Combining the ReHo and ALFF/fALFF data,the results revealed that the activity in the right cuneus and left precuneus was lower in the adolescent MDD patients than in the HCs(voxel size:648 mm3,P<0.05),and no brain region exhibited increased activity.Based on the ALFF data,we found decreased activity in the right cuneus and left precuneus in adolescent MDD patients(voxel size:736 mm3,P<0.05),with no regions exhibiting increased activity.CONCLUSION Through ALE meta-analysis,we consistently identified the right cuneus and left precuneus as vulnerable brain regions in adolescent MDD patients,increasing our understanding of the neuropathology of affected adolescents.

Multimodal abnormalities of brain structures in adolescents and young adults with major depressive disorder:An activation likelihood estimation meta-analysis

BACKGROUND Major depressive disorder(MDD)in adolescents and young adults contributes significantly to global morbidity,with inconsistent findings on brain structural changes from structural magnetic resonance imaging studies.Activation likeli-hood estimation(ALE)offers a method to synthesize these diverse findings and identify consistent brain anomalies.METHODS We performed a comprehensive literature search in PubMed,Web of Science,Embase,and Chinese National Knowledge Infrastructure databases for neuroi-maging studies on MDD among adolescents and young adults published up to November 19,2023.Two independent researchers performed the study selection,quality assessment,and data extraction.The ALE technique was employed to synthesize findings on localized brain function anomalies in MDD patients,which was supplemented by sensitivity analyses.RESULTS Twenty-two studies comprising fourteen diffusion tensor imaging(DTI)studies and eight voxel-based morphome-try(VBM)studies,and involving 451 MDD patients and 465 healthy controls(HCs)for DTI and 664 MDD patients and 946 HCs for VBM,were included.DTI-based ALE demonstrated significant reductions in fractional anisotropy(FA)values in the right caudate head,right insula,and right lentiform nucleus putamen in adolescents and young adults with MDD compared to HCs,with no regions exhibiting increased FA values.VBM-based ALE did not demonstrate significant alterations in gray matter volume.Sensitivity analyses highlighted consistent findings in the right caudate head(11 of 14 analyses),right insula(10 of 14 analyses),and right lentiform nucleus putamen(11 of 14 analyses).CONCLUSION Structural alterations in the right caudate head,right insula,and right lentiform nucleus putamen in young MDD patients may contribute to its recurrent nature,offering insights for targeted therapies.

Association between 5-HTR1A gene C-1019G polymorphism and antidepressant response in patients with major depressive disorder:A meta-analysis

BACKGROUND Major depressive disorder(MDD)is a substantial global health concern,and its treatment is complicated by the variability in individual response to antide-pressants.AIM To consolidate research and clarify the impact of genetic variation on MDD treatment outcomes.METHODS Adhering to Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines,a systematic search across PubMed,EMBASE,Web of Science,and the Cochrane Library was conducted without date restrictions,utilizing key terms related to MDD,serotonin 1A receptor polymorphism(5-HTR1A),C-1019G polymorphism,and antidepressant response.Studies meeting inclusion criteria were thoroughly screened,and quality assessed using the Newcastle-Ottawa Scale.Statistical analyses,includingχ2 and I²values,were used to evaluate heterogeneity and fixed-effect or random-effect models were applied accordingly.RESULTS The initial search yielded 1216 articles,with 11 studies meeting criteria for inclusion.Analysis of various genetic models showed no significant association between the 5-HTR1A C-1019G polymorphism and antidepressant efficacy.The heterogeneity was low to moderate,and no publication bias was detected through funnel plot symmetry and Egger's and Begg's tests.CONCLUSION This meta-analysis does not support a significant association between the 5-HTR1A C-1019G polymorphism and the efficacy of antidepressant treatment in MDD.The findings call for further research with larger cohorts to substantiate these results and enhance the understanding of antidepressant pharmacogenetics.

Cognitive Disorders, Depression and Anxiety in Temporal Lobe Epilepsy: An Overview

Partial epilepsies, originating in a specific brain region, affect about 60% of adults with epilepsy. Temporal lobe epilepsy (TLE) is the most prevalent subtype within this category, often necessitating surgical intervention due to its refractoriness to antiepileptic drugs (AEDs). Hippocampal sclerosis, a common underlying pathology, often exacerbates the severity by introducing cognitive and emotional challenges. This review delves deeper into the cognitive profile of TLE, along with the risk factors for cognitive disorders, depression, and anxiety in this population.

Reconsidering the role of depression and common psychiatric disorders as partners in the type 2 diabetes epidemic

Common psychiatric disorders(CPDs)and depression contribute significantly to the global epidemic of type 2 diabetes(T2D).We postulated a possible pathophysiological mechanism that through Bridge-Symptoms present in depression and CPDs,promotes the establishment of emotional eating,activation of the reward system,onset of overweight and obesity and,ultimately the increased risk of developing T2D.The plausibility of the proposed pathophysiological mechanism is supported by the mechanism of action of drugs such as naltrexonebupropion currently approved for the treatment of both obesity/overweight with T2D and as separate active pharmaceutical ingredients in drug addiction,but also from initial evidence that is emerging regarding glucagon-like peptide 1 receptor agonists that appear to be effective in the treatment of drug addiction.We hope that our hypothesis may be useful in interpreting the higher prevalence of CPDs and depression in patients with T2D compared with the general population and may help refine the integrated psychiatric-diabetic therapy approach to improve the treatment and or remission of T2D.

Death-associated protein kinase 1 is associated with cognitive dysfunction in major depressive disorder

We previously showed that death-associated protein kinase 1(DAPK1)expression is increased in hippocampal tissue in a mouse model of major depressive disorde and is related to cognitive dysfunction in Alzheimer's disease.In addition,depression is a risk factor for developing Alzheimer's disease,as well as an early clinical manifestation of Alzheimer's disease.Meanwhile,cognitive dysfunction is a distinctive feature of major depressive disorder.Therefore,DAPK1 may be related to cognitive dysfunction in major depressive disorder.In this study,we established a mouse model of major depressive disorder by housing mice individually and exposing them to chronic,mild,unpredictable stressors.We found that DAPK1 and tau protein levels were increased in the hippocampal CA3 area,and tau was hyperphosphorylated at Thr231,Ser262,and Ser396 in these mice.Furthermore,DAPK1 shifted from axonal expression to overexpression on the cell membrane.Exercise and treatment with the antidepressant drug citalopram decreased DAPK1 expression and tau protein phosphorylation in hippocampal tissue and improved both depressive symptoms and cognitive dysfunction.These results indicate that DAPK1 may be a potential reason and therapeutic target of cognitive dysfunction in major depressive disorder.

Meteorological factors, ambient air pollution, and daily hospital admissions for depressive disorder in Harbin: A time-series study

BACKGROUND The literature has discussed the relationship between environmental factors and depressive disorders;however,the results are inconsistent in different studies and regions,as are the interaction effects between environmental factors.We hypo-thesized that meteorological factors and ambient air pollution individually affect and interact to affect depressive disorder morbidity.AIM To investigate the effects of meteorological factors and air pollution on depressive disorders,including their lagged effects and interactions.METHODS The samples were obtained from a class 3 hospital in Harbin,China.Daily hos-pital admission data for depressive disorders from January 1,2015 to December 31,2022 were obtained.Meteorological and air pollution data were also collected during the same period.Generalized additive models with quasi-Poisson regre-ssion were used for time-series modeling to measure the non-linear and delayed effects of environmental factors.We further incorporated each pair of environ-mental factors into a bivariate response surface model to examine the interaction effects on hospital admissions for depressive disorders.RESULTS Data for 2922 d were included in the study,with no missing values.The total number of depressive admissions was 83905.Medium to high correlations existed between environmental factors.Air temperature(AT)and wind speed(WS)significantly affected the number of admissions for depression.An extremely low temperature(-29.0℃)at lag 0 caused a 53%[relative risk(RR)=1.53,95%confidence interval(CI):1.23-1.89]increase in daily hospital admissions relative to the median temperature.Extremely low WSs(0.4 m/s)at lag 7 increased the number of admissions by 58%(RR=1.58,95%CI:1.07-2.31).In contrast,atmospheric pressure and relative humidity had smaller effects.Among the six air pollutants considered in the time-series model,nitrogen dioxide(NO_(2))was the only pollutant that showed significant effects over non-cumulative,cumulative,immediate,and lagged conditions.The cumulative effect of NO_(2) at lag 7 was 0.47%(RR=1.0047,95%CI:1.0024-1.0071).Interaction effects were found between AT and the five air pollutants,atmospheric temperature and the four air pollutants,WS and sulfur dioxide.CONCLUSION Meteorological factors and the air pollutant NO_(2) affect daily hospital admissions for depressive disorders,and interactions exist between meteorological factors and ambient air pollution.

Kynurenine pathway of tryptophan metabolism in pathophysiology and therapy of major depressive disorder

Serotonin deficiency in major depressive disorder(MDD)has formed the basis of antidepressant drug development and was originally attributed to induction of the major tryptophan(Trp)-degrading enzyme,liver Trp 2,3-dioxygenase(TDO),by cortisol,leading to decreased Trp availability to the brain for serotonin synthesis.Subsequently,the serotonin deficiency was proposed to involve induction of the extrahepatic Trp-degrading enzyme indoleamine 2,3-dioxygenase(IDO)by proinflammatory cytokines,with inflammation being the underlying cause.Recent evidence,however,challenges this latter concept,as not all MDD patients are immune-activated and,when present,inflammation is mild and/or transient.A wide range of antidepressant drugs inhibit the activity of liver TDO and bind specifically to the enzyme,but not to IDO.IDO induction is not a major event in MDD,but,when it occurs,its metabolic consequences may be masked and overridden by upregulation of kynurenine monooxygenase(KMO),the gateway to production of modulators of immune and neuronal functions.KMO appears to be activated in MDD by certain proinflammatory cytokines and antidepressants with anti-inflammatory properties may block this activation.We demonstrate the ability of the antidepressant ketamine to dock(bind)to KMO.The pathophysiology of MDD may be underpinned by both the serotonin deficiency and glutamatergic activation mediated respectively by TDO induction and N-methyl-D-aspartate receptor activation.Inhibition of TDO and KMO should be the focus of MDD pharmacotherapy.

Major depressive disorder is correlated with the mitochondrial ND1 T3394C mutation in two Han Chinese families:Two case reports

BACKGROUND Major depressive disorder(MDD)is the most frequent reason of disabled people in the world,as reported by the World Health Organization.However,the diagnosis of MDD is mainly based on clinical symptoms.CASE SUMMARY The clinical,genetic,and molecular characteristics of two Chinese families with MDD are described in this study.There were variable ages of onset and severity in depression among the families.Both Chinese families had a very low prevalence of MDD.The mitochondrial genomes of these pedigrees were sequenced and indicated a homoplasmic T3394C(Y30H)mutation,with the polymorphism located at a highly conserved tyrosine at position 30 of ND1.The analysis also revealed unique sets of mitochondrial DNA(mtDNA)polymorphisms originating from haplogroups M9a3 and M9a.CONCLUSION This finding of the T3394C mutation in two unrelated depressed patients provides strong evidence that this mutation may have a part in the etiology of MDD.However,In these two Chinese families having the T3394C mutation,no functional mt DNA mutation was observed.Therefore,T3394C mutations are related with MDD,and the phenotypic manifestation of these mutations may be affected by changes in nuclear genes or environmental factors.

Identification and characterization of noncoding RNAs-associated competing endogenous RNA networks in major depressive disorder

BACKGROUND Major depressive disorder(MDD)is a common and serious mental illness.Many novel genes in MDD have been characterized by high-throughput methods such as microarrays or sequencing.Recently,noncoding RNAs(ncRNAs)were suggested to be involved in the complicated environmental-genetic regulatory network of MDD occurrence;however,the interplay among RNA species,including protein-coding RNAs and ncRNAs,in MDD remains unclear.AIM To investigate the RNA expression datasets downloaded from a public database and construct a network based on differentially expressed long noncoding RNA(lncRNAs),microRNAs(miRNAs),and mRNAs between MDD and controls.METHODS Gene expression data were searched in NCBI Gene Expression Omnibus using the search term“major depressive disorder.”Six array datasets from humans were related to the search term:GSE19738,GSE32280,GSE38206,GSE52790,GSE76826,and GSE81152.These datasets were processed for initial assessment and subjected to quality control and differential expression analysis.Differentially expressed lncRNAs,miRNAs,and mRNAs were determined,Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed,and protein-protein interaction network was generated.The results were analyzed for their association with MDD.RESULTS After analysis,3 miRNAs,12 lncRNAs,and 33 mRNAs were identified in the competing endogenous RNA network.Two of these miRNAs were earlier shown to be involved in psychiatric disorders,and differentially expressed mRNAs were found to be highly enriched in pathways related to neurogenesis and neuroplasticity as per Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses.The expression of hub gene fatty acid 2-hydroxylase was enriched,and the encoded protein was found to be involved in myelin formation,indicating that neurological development and signal transduction are involved in MDD pathogenesis.CONCLUSION The present study presents candidate nc RNAs involved in the neurogenesis and neuroplasticity pathways related to MDD.

Effects of mindfulness-based interventions on depressive symptoms in patients with substance use disorders:a systematic review and meta-analysis

Objective:We examined the effects of mindfulness-based interventions(MBIs)on depressive symptoms in patients with substance use disorders(SUDs)and explored the moderating effects of participant,method,and intervention characteristics.Methods:We systematically searched 8 databases from their inception till November 2021.The inclusion criteria were primary studies evaluating MBIs in patients with SUDs with depression measured as an outcome,those including a control group,and those written in English.We used a random-effects model to compute effect sizes(ESs)using Hedges’g,a forest plot,and Q and I2 statistics as measures of heterogeneity;we also examined moderator analyses.Results:Nineteen studies included 1352 participants(age:38.6±7.0 years).Overall,MBIs showed significantly improved depression(g=0.67,95%confidence interval[CI]:0.29,1.05,I2=89%)compared to controls.With regard to moderators,providing MBIs as an individual plus group intervention had a greater effect(g=2.13)on reducing depressive symptoms than providing MBIs as a group intervention(g=0.64)or an individual intervention only(g=0.33,P=0.034).Using concealed allocation tended to reduce depressive symptoms(g=1.22)as compared to not using concealed allocation(g=0.48,P=0.086).No other quality indicators were demonstrated to have a moderating influence on the value of the ES.Conclusions:MBIs improved depressive symptoms in patients with SUDs.MBIs might be used as an adjunctive or alternative to conventional treatment for depressed patients with SUDs.

Intestinal flora and depressive disorders:exploration and prospect of microbial-gut-brain axis

This paper examines the correlation between depressive disorders and intestinal flora.Depression is a common affective disorder characterized by low mood,loss of interest,anhedonia,high incidence,high recurrence rate,high disability rate,and high medical costs.The incidence and harmfulness of depressive disorder are gradually increasing,and its etiology is complex and diverse,among which the abnormal intestinal flora is considered to be one of the causes of depressive disorder.This article reviews the results of several studies that found intestinal flora imbalance in depressed patients,including changes in the type and quantity of flora and changes in metabolic pathways.In addition,antibiotic and probiotic treatments have also been shown to be effective in alleviating depressive symptoms,further indicating the importance of intestinal flora disturbances in the pathogenesis of depression.We also explored the relationship between intestinal flora and the pathogenesis of depressive disorders.Through neuro-immuno-endo-crine-metabolic pathways,intestinal flora can affect the function of the central nervous system,cause changes in the host’s mental behavior,and lead to or aggravate depressive symptoms.Overall,this study not only found differences in the intestinal flora of patients with depressive disorders but also revealed the potential role of intestinal flora in the pathogenesis.Importantly,this provides a new theoretical basis for further clarifying the pathogenesis of depressive disorders and formulating diagnosis and treatment strategies.

Research progress on the effects of positive stress reduction on positive awareness and psychosocial functioning in patients with depressive disorders

To review the current research status of positive thought stress reduction therapy(PTSRT),psychosocial functioning of patients with depressive disorders,the shortcomings and outlook of the influence of PTSRT on positive thought awareness,and psychosocial functioning of patients with depressive disorders.This review has the objective to provide clinical healthcare personnel with essential information about the use of PTSRT to improve the level of positive thought and psychosocial functioning of patients with depressive disorders.

Mechanism of Zuojin Pill in the treatment of anxiety disorder and Major depressive disorder based on network pharmacology and molecular docking validation

Background:Zuojin Pill(ZJP)is a classic Chinese herbal prescription with good efficacy in the treatment of Anxiety disorder(AD)and Major depressive disorder(MDD).Nevertheless,the potential mechanisms of ZJP remain unclear.Based on network pharmacology and molecular docking methods,this study aims to elucidate the possible mechanism of ZJP in the treatment of AD and MDD.Methods:The components and targets of Rhizoma Coptidis and Fructus Evodiae were collected from TCMSP,ETCM,HERB,SWISSADME and STITCH databases.The disease targets related to MDD and AD were collected from DISGENET,GENECARDS and OMIM databases.Protein-protein interaction network was constructed by STRING database,GO and KEGG enrichment analysis was performed by METASCAPE database,and“drugs-components-targets network”was constructed by Cytoscape software.Molecular docking verification was performed by Sailvina2.0 software.Results:ZJP may act on AKT1,IL6,TNF and other targets through caffeine,isorhamnetin,berberine and other components,regulating the Inflammatory mediator regulation of TRP channels,Serotonergic synapse,Dopaminergic synapse,PI3K/AKT signaling pathway,and other pathways.The results of molecular docking showed that berberine had the best binding activity with the core target.Conclusion:ZJP can exert anti-anxiety and anti-depression effects through multiple components,multiple targets and multiple pathways.

Targeting TrkB–PSD-95 coupling to mitigate neurological disorders

Tropomyosin receptor kinase B(TrkB)signaling plays a pivotal role in dendritic growth and dendritic spine formation to promote learning and memory.The activity-dependent release of brain-derived neurotrophic factor at synapses binds to pre-or postsynaptic TrkB resulting in the strengthening of synapses,reflected by long-term potentiation.Postsynaptically,the association of postsynaptic density protein-95 with TrkB enhances phospholipase Cγ-Ca^(2+)/calmodulin-dependent protein kinaseⅡand phosphatidylinositol 3-kinase-mechanistic target of rapamycin signaling required for long-term potentiation.In this review,we discuss TrkB-postsynaptic density protein-95 coupling as a promising strategy to magnify brain-derived neurotrophic factor signaling towards the development of novel therapeutics for specific neurological disorders.A reduction of TrkB signaling has been observed in neurodegenerative disorders,such as Alzheimer's disease and Huntington's disease,and enhancement of postsynaptic density protein-95 association with TrkB signaling could mitigate the observed deficiency of neuronal connectivity in schizophrenia and depression.Treatment with brain-derived neurotrophic factor is problematic,due to poor pharmacokinetics,low brain penetration,and side effects resulting from activation of the p75 neurotrophin receptor or the truncated TrkB.T1 isoform.Although TrkB agonists and antibodies that activate TrkB are being intensively investigated,they cannot distinguish the multiple human TrkB splicing isoforms or cell type-specific functions.Targeting TrkB–postsynaptic density protein-95 coupling provides an alternative approach to specifically boost TrkB signaling at localized synaptic sites versus global stimulation that risks many adverse side effects.

From Signals to Solutions: Exploring Early Detection of Neuropsychiatric and Neurodevelopment Disorders through Biomarkers

In 2013, the percentage of children ranging from 5 to 17 years who reported being diagnosed with autism surged to 1.2% from 0.1% in 1997 [1]. Alongside this increase in the incidence of autism in children, there were findings of a 21% increase in children who displayed behavioral and conduct problems from 2019 to 2020 [2]. Early detection of neuropsychiatric and neurodevelopmental disorders in children is critical for timely intervention and improved long-term outcomes. With early intervention, there is better aptitude to support healthy development and give proper treatment to attain a better quality of life. This paper explores studies aimed at enhancing the early detection of these disorders through the use of biomarkers with the aim of creating a bridge between the worlds of research and clinical practice. The disorders in this paper specifically discussed are Major Depressive Disorder, Bipolar Disorder, and Autism Spectrum Disorder. With this bridge, we can foster collaborations and encourage further advancement in the field of early detection and intervention.

Clarifying the relationship and analyzing the influential factors of bronchial asthma in children with attention-deficit hyperactivity disorder

BACKGROUND Bronchial asthma is closely related to the occurrence of attention-deficit hyperactivity disorder(ADHD)in children,which can easily have adverse effects on children’s learning and social interactions.Studies have shown that childhood asthma can increase the risk of ADHD and the core symptoms of ADHD.Compared with children with ADHD alone,children with asthma and ADHD are more likely to show high levels of hyperactivity,hyperactive-impulsive and other externalizing behaviors and anxiety in clinical practice and have more symptoms of somatization and emotional internalization.AIM To explore the relationship between ADHD in children and bronchial asthma and to analyze its influencing factors.METHODS This retrospective cohort study was conducted at Dongying People's Hospital from September 2018 to August 2023.Children diagnosed with ADHD at this hospital were selected as the ADHD group,while healthy children without ADHD who underwent physical examinations during the same period served as the control group.Clinical and parental data were collected for all participating children,and multivariate logistic regression analysis was employed to identify risk factors for comorbid asthma in children with ADHD.RESULTSSignificant differences were detected between the ADHD group and the control group in terms of family history ofasthma and allergic diseases, maternal complications during pregnancy, maternal use of asthma and allergymedications during pregnancy, maternal anxiety and depression during pregnancy, and parental relationshipstatus (P < 0.05). Out of the 183 children in the ADHD group, 25 had comorbid asthma, resulting in a comorbidityrate of 13.66% (25/183), compared to the comorbidity rate of 2.91% (16/549) among the 549 children in the controlgroup. The difference in the asthma comorbidity rate between the two groups was statistically significant (P <0.05). The results of the multivariate logistic regression analysis indicated that family history of asthma and allergicdiseases, maternal complications during pregnancy, maternal use of asthma and allergy medications duringpregnancy, maternal anxiety and depression during pregnancy, and parental relationship status are independentrisk factors increasing the risk of comorbid asthma in children with ADHD (P < 0.05).CONCLUSIONChildren with ADHD were more likely to have comorbid asthma than healthy control children were. A familyhistory of asthma, adverse maternal factors during pregnancy, and parental relationship status were identified asrisk factors influencing the comorbidity of asthma in children with ADHD. Clinically, targeted interventions basedon these factors can be implemented to reduce the risk of comorbid asthma. This information is relevant for resultssections of abstracts in scientific articles.

Evaluating Pharmacological and Rehabilitation Strategies for Effective Management of Bipolar Disorder: A Comprehensive Clinical Study

Bipolar disorder presents significant challenges in clinical management, characterized by recurrent episodes of depression and mania often accompanied by impairment in functioning. This study investigates the efficacy of pharmacological interventions and rehabilitation strategies to improve patient outcomes and quality of life. Utilizing a randomized controlled trial with multiple treatment arms, participants will receive pharmacotherapy, polypharmacotherapy, rehabilitation interventions, or combination treatments. Outcome measures will be assessed using standardized scales, including the Hamilton Depression Scale, Yale-Brown Obsessive Compulsive Scale (Y-BOCS), and Mania Scale. Preliminary data suggest improvements in symptom severity and functional outcomes with combination treatments. This research aims to inform clinical practice, guide treatment decisions, and ultimately enhance the quality of care for individuals living with bipolar disorder. Findings will be disseminated through peer-reviewed journals and scientific conferences to advance knowledge in this field.