Causal role of immune cells in bipolar disorder: a Mendelian randomization study DOI Creative Commons

M. Wang,

Shuo Wang,

Guoshan Yuan

и другие.

Frontiers in Psychiatry, Год журнала: 2024, Номер 15

Опубликована: Авг. 16, 2024

Background The understanding of the immunological mechanisms underlying bipolar disorder (BD) has enhanced in recent years due to extensive use high-density genetic markers for genotyping and advancements genome-wide association studies (GWAS). However, on relationship between immune cells risk BD remain limited, necessitating further investigation. Methods Bidirectional two-sample Mendelian Randomization (MR) analysis was employed investigate causal cell morphologies disorder. Immune traits were collected from a research cohort Sardinia, whereas GWAS summary statistics obtained Psychiatric Genomics Consortium. Sensitivity analyses conducted, combination MR-Egger MR-Presso used assess horizontal pleiotropy. Cochran’s Q test evaluate heterogeneity, results adjusted false discovery rate (FDR). Results study identified six phenotypes significantly associated with incidence ( P < 0.01). These include IgD- CD27- %lymphocyte, CD33br HLA DR+ CD14- AC, CD8 CD28+ CD45RA+ CD8br, CD14 CD14+ CD16+ monocyte, HVEM CD45RA- CD4+. After adjusting FDR 0.2, two remained statistically significant: IgD-CD27-% lymphocyte (OR=1.099, 95% CI: 1.051-1.149, = 3.51E-05, FDR=0.026) CD14-AC (OR=0.981, 0.971-0.991, 2.17E-04, FDR=0.079). In reverse MR analysis, impacted four monocytes 0.01), including CD64 CX3CR1 CD16-, CD16- monocyte. after applying correction (FDR 0.2), no significant observed. Conclusions This investigation reveals associations phenotypes, disorder, genetics, providing novel perspectives prospective therapeutic targets

Язык: Английский

Inflammatory mediators in major depression and bipolar disorder DOI Creative Commons
Sara Poletti, Mario Gennaro Mazza, Francesco Benedetti

и другие.

Translational Psychiatry, Год журнала: 2024, Номер 14(1)

Опубликована: Июнь 8, 2024

Abstract Major depressive disorder (MDD) and bipolar (BD) are highly disabling illnesses defined by different psychopathological, neuroimaging, cognitive profiles. In the last decades, immune dysregulation has received increasing attention as a central factor in pathophysiology of these disorders. Several aspects dysregulations have been investigated, including, low-grade inflammation cytokines, chemokines, cell populations, gene expression, markers both peripheral activation. Understanding distinct profiles characterizing two disorders is indeed crucial importance for differential diagnosis implementation personalized treatment strategies. this paper, we reviewed current literature on response system focusing our studies using inflammatory to discriminate between MDD BD. High heterogeneity characterized available literature, reflecting Common alterations include high pro-inflammatory cytokines such IL-6 TNF-α. On contrary, greater involvement chemokines associated with innate immunity reported BD together dynamic changes T cells differentiation defects during childhood which normalize adulthood, whereas classic mediators responses IL-4 IL-10 present signs immune-senescence.

Язык: Английский

Процитировано

33

The immunological perspective of major depressive disorder: unveiling the interactions between central and peripheral immune mechanisms DOI Creative Commons
Jiao Wang, Jiayi Lin,

Yanfang Deng

и другие.

Journal of Neuroinflammation, Год журнала: 2025, Номер 22(1)

Опубликована: Янв. 19, 2025

Major depressive disorder is a prevalent mental disorder, yet its pathogenesis remains poorly understood. Accumulating evidence implicates dysregulated immune mechanisms as key contributors to disorders. This review elucidates the complex interplay between peripheral and central components underlying pathology. Peripherally, systemic inflammation, gut dysregulation, dysfunction in organs including gut, liver, spleen adipose tissue influence brain function through neural molecular pathways. Within nervous system, aberrant microglial astrocytes activation, cytokine imbalances, compromised blood-brain barrier integrity propagate neuroinflammation, disrupting neurotransmission, impairing neuroplasticity, promoting neuronal injury. The crosstalk immunity creates vicious cycle exacerbating neuropathology. Unraveling these multifaceted immune-mediated provides insights into major disorder's pathogenic basis potential biomarkers targets. Modulating both responses represent promising multidimensional therapeutic strategy.

Язык: Английский

Процитировано

5

Linking depression and neuroinflammation: crosstalk between glial cells DOI
Xueying Yang, Huiqin Wang, Zhen‐Zhen Wang

и другие.

European Journal of Pharmacology, Год журнала: 2025, Номер unknown, С. 177408 - 177408

Опубликована: Фев. 1, 2025

Язык: Английский

Процитировано

1

Anhedonia: Current and future treatments DOI Creative Commons
Alessandro Serretti

Psychiatry and Clinical Neurosciences Reports, Год журнала: 2025, Номер 4(1)

Опубликована: Март 1, 2025

Abstract Anhedonia is a transdiagnostic domain that leads to poor disorder outcome and low remission rates. This narrative review describes broad range of interventions targeting anhedonia, including pharmacological, neuromodulatory, behavioral, lifestyle‐based approaches. Drugs such as vortioxetine, agomelatine, bupropion, ketamine, brexpiprazole show promising anti‐anhedonic effects, while traditional antidepressants, serotonin‐norepinephrine reuptake inhibitors (SNRIs) and, even more so, selective serotonin (SSRIs), are less effective. Neuromodulation techniques, repetitive transcranial magnetic stimulation, direct current transcutaneous auricular vagus nerve proved effective at improving particularly when used in targeted areas. Psychotherapeutic interventions, behavioral activation, mindfulness‐based strategies, savoring also help re‐engage patients with pleasurable activities enhance positive affect. Innovative treatments, aticaprant psilocybin, showed results. Substantial evidence suggests anhedonia better psychosocial functioning, quality life, sustained remission. Although most data come from short‐term studies, several long‐term analyses suggest maintaining hedonic improvements feasible beneficial. The reviewed underscores the importance routine assessment integration symptom‐specific strategies. Tailoring address individual patterns reward disruption may optimize outcomes for anhedonia.

Язык: Английский

Процитировано

1

Pharmacotherapeutic value of inflammatory and neurotrophic biomarkers in bipolar disorder: A systematic review DOI Creative Commons

Paloma Ruiz-Sastre,

Carlos Gómez Sánchez-Lafuente, Jaime Martín‐Martín

и другие.

Progress in Neuro-Psychopharmacology and Biological Psychiatry, Год журнала: 2024, Номер 134, С. 111056 - 111056

Опубликована: Июнь 13, 2024

The various pharmacological interventions, ranging from mood stabilizers and antipsychotics to antidepressants, reflect the diff/iculty of treating depressive/manic symptomatology bipolar disorder (BD). Among a broad range mechanisms implicated, immune dysregulation may contribute increased inflammation that influences course BD. Inflammatory, neurotrophic oxidative stress factors be identified as promising peripheral biomarkers in brain functioning, perhaps serving predictors an effective response treatment for present systematic review aimed examine evidence supporting pharmacotherapeutic value inflammatory PubMed, PsychINFO, Scopus Web Science were searched inception May 2024 by two independent reviewers. A total 40 studies with 3371 patients diagnosis intervention BD selected. Inconsistencies effects treatments on connection between expected anti-inflammatory symptomatologic improvement identified. Mood (lithium), (quetiapine), antidepressants (ketamine) or their combination described increase both pro-inflammatory (TNFα, IL-6) (IL-4, IL-8) factors. Other medications, such memantine dextromethorphan, autoimmune (infliximab) non-steroidal (aspirin, celecoxib) drugs, antidiabetics (pioglitazone), even dietary supplementation (omega-3), combination, clearly decrease IL-6, IL-1β, C-reactive protein) and/or factor BDNF patients. Inflammation requires further investigation understand underlying immunologic mechanism, identify response, make informed decisions about use development more interventions

Язык: Английский

Процитировано

4

Low-dose interleukin-2 in patients with bipolar depression: A phase 2 randomised double-blind placebo-controlled trial DOI
Marion Leboyer, Marianne Foiselle, Nicolas Tchitchek

и другие.

Brain Behavior and Immunity, Год журнала: 2024, Номер 123, С. 177 - 184

Опубликована: Сен. 4, 2024

Язык: Английский

Процитировано

3

Indications for an antidepressive effect of thymosin alpha-1 in a small open-label proof of concept study in Common Variable Immune Deficiency patients with depression. DOI Creative Commons
D Mersha,

Sarah E. Fromme,

Frank van Boven

и другие.

Brain Behavior & Immunity - Health, Год журнала: 2025, Номер 43, С. 100934 - 100934

Опубликована: Янв. 5, 2025

A considerable proportion (21%) of patients with common variable immunodeficiency (CVID) suffers from depression. These subjects are characterized by reduced naïve T cells and a premature cell senescence similar to that major depressive disorder (MDD). It is known essential for limbic system development/function. Treatment thymosin α1 (Tα1) capable increase the thymus output cells. To treat CVID comorbid episode Tα1 thereby improve mood. small open-label, proof concept trial. Five depressed (Hamilton Depression Rating Scale, HDRS >12) could be treated (8 weeks, 1.6 mg daily subcutaneously, 1st week, thereafter twice weekly). At start, at 8 weeks after last injection, was recorded blood samples drawn measuring memory cells, Th17 Treg hsCRP, IL-6 IL-7. Outcomes were compared those contrast group (42 MDD patients, same severity but as usual (TAU)). In all 5 decreased during treatment (with average 52%, TAU scores 36% in patients). All showed an naïve/memory CD4+ CD8+ ratios, 4 detectable levels reductions recorded. did not show such immune improvements. 8-week wash-out, depression recurred 2 most severe while continued others. Immune effects sustained wash-out. This preliminary study suggests hormone have antidepressive related correcting effects. Data urge larger placebo-controlled trials.

Язык: Английский

Процитировано

0

Chipping away at the iceberg: Uncovering immune complexity in schizophrenia DOI
Fabiana Corsi‐Zuelli

Brain Behavior and Immunity, Год журнала: 2025, Номер 125, С. 410 - 412

Опубликована: Фев. 2, 2025

Язык: Английский

Процитировано

0

Effects of kynurenine pathway metabolites on choroid plexus volume, hemodynamic response, and spontaneous neural activity: A new mechanism for disrupted neurovascular communication and impaired cognition in mood disorders DOI
B. Bravi, Chiara Vitale,

Palladini Mariagrazia

и другие.

Brain Behavior and Immunity, Год журнала: 2025, Номер 125, С. 414 - 427

Опубликована: Фев. 3, 2025

Язык: Английский

Процитировано

0

Fibromyalgia, Depression, and Autoimmune Disorders: An Interconnected Web of Inflammation DOI Creative Commons
Stefania Sedda, Maria Piera L. Cadoni, Serenella Medici

и другие.

Biomedicines, Год журнала: 2025, Номер 13(2), С. 503 - 503

Опубликована: Фев. 18, 2025

Background: Fibromyalgia, depression, and autoimmune diseases represent a triad of interconnected conditions characterized by overlapping biological pathways, including chronic inflammation, immune dysregulation, neurochemical imbalances. Understanding their shared mechanisms offers opportunities for innovative therapeutic approaches. Objective: This systematic review explores the common inflammatory- immune-related pathways among these conditions, emphasizing implications biomarker development novel strategies. Methods: Following PRISMA guidelines, comprehensive literature search was conducted in databases PubMed, Scopus, Web Science, Cochrane Library. Studies examining relationship between fibromyalgia, with focus on responses, inflammatory biomarkers, interventions were included. The quality selected studies assessed using Risk Bias tool. Results: From 255 identified studies, 12 met inclusion criteria. Evidence supports role pro-inflammatory cytokines (e.g., IL-6, TNF-α) dysregulation serotonin, dopamine) as key factors pathophysiology conditions. Pilot highlight potential immune-modulating therapies, low-dose IL-2 anti-inflammatory agents such N-acetylcysteine minocycline, alleviating both physical psychological symptoms. Emerging cytokine profiles platelet serotonin activity, show promise personalized treatment Conclusions: linking underscore need integrated Although pilot provide preliminary insights, validation through large-scale, multicenter trials is essential. Future research should standardizing methodologies leveraging biomarker-driven precision medicine to improve outcomes patients complex, multifactorial

Язык: Английский

Процитировано

0