Ceylan, Deniz

Background/Objectives: Mood disorders, such as major depressive disorder (MDD) and bipolar disorder (BD), along with obstructive sleep apnea (OSA), are prevalent conditions that have serious effects on affected individuals and public health. These issues have received more attention recently, as research shows there are similar risk factors and they can influence each other by worsening symptoms and treatment response. However, there is still no clear understanding of the extent of this co-occurrence and the factors that influence it. Methods: A systematic review of comorbid OSA and mood disorders was conducted from EMBASE, Ovid MEDLINE, Global Health, and APA PsycINFO (1 January 2013–25 July 2025), with meta-analyses applying random-effects models in R (metafor). Heterogeneity, publication bias, subgroup effects, and meta-regression analyses were performed by assessing demographic, clinical, and study quality variables. Results: Out of 6221 screened studies, 23 articles met eligibility criteria, yielding 2,380,986 OSA patients, with 446,495 comorbid mood disorders (MDD = 446,290; BD = 205), and 5724 mood disorder patients (MDD = 1987; BD = 3737) with 450 comorbid OSA. All meta-analyses demonstrated a significant prevalence of comorbidity, accompanied by substantial heterogeneity. Meta-regression analyses identified mean age (β = 0.18, 95% CI 0.03–0.33, p = 0.02) and mean body mass index (β = −0.18, 95% CI −0.32 to −0.04, p = 0.01) as significant moderators of OSA prevalence. Conclusions: This meta-analysis indicates a high prevalence of comorbidity between OSA and mood disorders, including MDD and BD, with significant heterogeneity. Age and body mass index emerged as significant moderators of OSA prevalence, emphasizing the need for systematic screening and tailored approaches in both clinical practice and research.

Abstract Introduction Bipolar disorder (BD) has been associated with increased medical burden and accelerated biological aging. Long non-coding RNAs (lncRNAs) regulate molecular pathways related to cellular senescence, inflammation, and telomere maintenance, which are implicated in both BD and aging. This study examined whether aging-related lncRNA expression reflects familial vulnerability or illness-specific effects, and whether childhood trauma and lifestyle factors modulate these signatures within a gene–environment framework. Methods In this cross-sectional study, expression levels of aging-related lncRNAs, including Antisense Non-coding RNA in the INK4 Locus (ANRIL), HOX Transcript Antisense Intergenic RNA (HOTAIR), Nuclear Enriched Abundant Transcript 1 (NEAT1), Taurine Upregulated Gene 1 (TUG1), Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1), Growth Arrest-Specific 5 (GAS5), and Telomerase RNA Component (TERC), were measured in peripheral blood mononuclear cells (PBMCs) from individuals with bipolar disorder (BD) (n=68), siblings without BD diagnosis (SIB) (n=54), and healthy controls (HC) (n=70) using quantitative reverse transcription polymerase chain reaction (RT-qPCR). Childhood trauma and lifestyle were assessed using the Childhood Trauma Questionnaire (CTQ) and the Healthy Lifestyle Profile II (HPLP-II). Principal component analysis generated a composite aging-related lncRNA factor. Results At the individual transcript level, NEAT1 and TERC were elevated, whereas GAS5 was reduced, in both BD and SIB relative to HC. The aging-related lncRNA composite score was higher in BD and SIB than in HC (F = 7.315, p = 0.001). Familial liability to BD (presence vs. absence of familial liability ) showed a significant main effect on the composite score (F(1,182)=8.18, p=0.005) and interacted with childhood trauma (F(1,182)=10.14, p=0.002). In multivariable models, total CTQ and physical neglect were independently associated with lower composite scores, while familial liability remained a positive predictor (all p<0.001). Conclusions Aging-related lncRNA alterations mark familial vulnerability to BD and are shaped by childhood trauma within a gene–environment interaction framework.

AbstractIntroductionThe immune system's inflammatory response, driven by pro-inflammatory proteins, protects against external threats. Fear and disgust-inducing stimuli have been linked to immune responses, yet their specific physiological and inflammatory mechanisms in trypophobia remain unclear. This study aimed to elucidate the inflammatory and physiological responses in relation to natural (non-skin) and skin-related trypophobic images.Material and methodsFifty participants (n = 50) were recruited for the study, and their sensitivity to trypophobia was measured using the trypophobia questionnaire. Then, participants were randomly assigned to either the skin related or non-skin related visual exposure group and viewed trypophobic images from a computer screen. Blood samples were collected pre- and post-exposure to trypophobic images and analyzed for IL-6 and TNF-α using ELISA and RT-qPCR methods.ResultsIL-6 and TNF-α protein levels significantly increased post-exposure, with IL-6 changes varying by stimulus type. mRNA expression showed significant interaction with participants' trypophobia sensitivity scores, suggesting post-transcriptional mechanisms. Heart rate variability (HRV) and heart rate were measured before, during, and after exposure using photoplethysmography. Significant changes in HRV metrics, influenced by stimulus type and trypophobia sensitivity, indicated increased sympathetic and decreased parasympathetic nervous system activity during and after exposure.ConclusionsThese findings highlight the role of physiological and inflammatory responses in trypophobia, suggesting immune activation and autonomic nervous system involvement based on stimulus type and individual sensitivity. These findings not only contribute to phobia literature but also shed light on the physiological and immunological changes that take place in the bodies of individuals with high sensitivity to trypophobia.

Suicide is a major public health concern; nevertheless, its neurobiology remains unknown. An area of interest in suicide research is the dorsolateral prefrontal cortex (DLPFC). We aimed to identify altered proteins and potential biological pathways in the DLPFC of individuals who died by suicide employing mass spectrometry-based untargeted proteomics. Postmortem DLPFC from age-matched male suicide mood disorder cases (n = 5) and non-suicide mood disorder cases (n = 5) were compared. The proteins that differed between groups at false discovery rate (FDR) adjusted p-values (Benjamini–Hochberg–Yekutieli) <0.3 and Log2 fold change (FC) >|0.4| were considered statistically significant and were subjected to pathway analysis by Qiagen Ingenuity software. Thirty-three of the 5162 detected proteins showed significantly altered expression levels in the suicide cases and two of them after adjustment for body mass index. The top differentially expressed protein was potassium voltage-gated channel subfamily Q member 3 (KCNQ3) (Log2FC = −0.481, p = 2.10 × 10−09, FDR = 5.93 × 10−06), which also showed a trend to downregulation in Western blot (p = 0.045, Bonferroni adjusted p = 0.090). The most notably enriched pathway was the GABA receptor signaling pathway (p < 0.001). Here, we report a reduction trend of KCNQ3 levels in the DLPFC of male suicide victims with mood disorders. Further studies with a larger sample size and equal sex representation are needed.