Infantile Amnesia can be Operationalized as a Psychological Meta Norm in the Development of Memory DOI Creative Commons

Bozhidara Stoencheva,

Kristina Stoyanova, Drozdstoy Stoyanov

et al.

Journal of Integrative Neuroscience, Journal Year: 2025, Volume and Issue: 24(2)

Published: Feb. 10, 2025

This paper offers a syncretic synthesis of the highlights scientific knowledge accumulated to date on mechanisms infantile amnesia (IA). IA can be conceptualized as meta-norm memory development. The review shows that neurobiological and neuropsychological evidence for converges within common metacognitive framework inquiry. involvement consciousness in conditioning traces association between implicit allow analyzed phenomenon with complex, universal neuropsychic regulation higher order. approach overcomes paradox understanding IA.

Language: Английский

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

et al.

Journal of Neuroinflammation, Journal Year: 2025, Volume and Issue: 22(1)

Published: Jan. 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.

Language: Английский

Citations

5
Pro-inflammatory cytokines in stress-induced depression: Novel insights into mechanisms and promising therapeutic strategies DOI
Jun Chang,

Tingcan Jiang,

Xiaoqian Shan

et al.

Progress in Neuro-Psychopharmacology and Biological Psychiatry, Journal Year: 2024, Volume and Issue: 131, P. 110931 - 110931

Published: Jan. 2, 2024

Language: Английский

Citations

15
“Inflamed” depression: A review of the interactions between depression and inflammation and current anti-inflammatory strategies for depression DOI Creative Commons

Yishu Yin,

Ting Ju,

Deyong Zeng

et al.

Pharmacological Research, Journal Year: 2024, Volume and Issue: 207, P. 107322 - 107322

Published: July 20, 2024

Depression is a common mental disorder, the effective treatment of which remains challenging issue worldwide. The clinical pathogenesis depression has been deeply explored, leading to formulation various pathogenic hypotheses. Among these, monoamine neurotransmitter hypothesis holds prominent position, yet it significant limitations as more than one-third patients do not respond conventional treatments targeting transmission disturbances. Over past few decades, growing body research highlighted link between inflammation and potential key factor in pathophysiology depression. In this review, we first summarize relationship depression, with focus on pathophysiological changes mediated by mechanisms linking well multiple anti-inflammatory strategies are also discussed, their efficacy safety assessed. This review broadens perspective specific aspects using for treating laying groundwork advancing precision medicine individuals suffering from "inflamed"

Language: Английский

Citations

15
Role of Glial Cells in Neuronal Function, Mood Disorders, and Drug Addiction DOI Creative Commons
Yousef Tizabi, Bruk Getachew, Sheketha R. Hauser

et al.

Brain Sciences, Journal Year: 2024, Volume and Issue: 14(6), P. 558 - 558

Published: May 30, 2024

Mood disorders and substance use disorder (SUD) are of immense medical social concern. Although significant progress on neuronal involvement in mood reward circuitries has been achieved, it is only relatively recently that the role glia these attracted attention. Detailed understanding glial functions devastating diseases could offer novel interventions. Here, following a brief review involved regulation perception, specific contributions neurotrophic factors, neuroinflammation, gut microbiota to highlighted. In this context, cells (e.g., microglia, astroglia, oligodendrocytes, synantocytes) phenotypic manifestation or SUD emphasized. addition, knowledge potential development therapeutics touched upon.

Language: Английский

Citations

13
Estrogen-immuno-neuromodulation disorders in menopausal depression DOI Creative Commons

Yuling Zhang,

Xiying Tan,

Chaozhi Tang

et al.

Journal of Neuroinflammation, Journal Year: 2024, Volume and Issue: 21(1)

Published: June 19, 2024

Abstract A significant decrease in estrogen levels puts menopausal women at high risk for major depression, which remains difficult to cure despite its relatively clear etiology. With the discovery of abnormally elevated inflammation depressed women, immune imbalance has become a novel focus study depression. In this paper, we examined characteristics and possible mechanisms caused by decreased during menopause found that deficiency disrupted homeostasis, especially inflammatory cytokines through ERα/ERβ/GPER-associated NLRP3/NF-κB signaling pathways. We also analyzed destruction blood-brain barrier, dysfunction neurotransmitters, blockade BDNF synthesis, attenuation neuroplasticity cytokine activity, investigated estrogen-immuno-neuromodulation disorders Current research suggests drugs targeting molecules are promising restoring homeostasis system may play positive role intervention treatment

Language: Английский

Citations

9
From air to mind: unraveling the impact of indoor pollutants on psychiatric disorders DOI Creative Commons
Germán Torres,

Ryia T. Subbaiah,

Riya A. Sood

et al.

Frontiers in Psychiatry, Journal Year: 2025, Volume and Issue: 15

Published: Jan. 9, 2025

Epidemiological evidence from the past 20 years indicates that environmental chemicals brought into air by vaporization of volatile organic compounds and other anthropogenic pollutants might be involved, at least in part, development or progression psychiatric disorders. This comes primarily occupational work studies humans, with indoor occupations being most important sources airborne affecting neural circuits implicated mood disorders (e.g., major depressive disorder bipolar disorder). The current mini review brings together recent findings pollution different fields research, including genetics, neuropathology, neuroimaging, for gauging underlying physiological mechanisms leading to emotional disturbances impact nearly all aspects human behavior. A better understanding how affect brain neurons augment clinical symptoms associated will undoubtedly useful subsequent treatment patients and/or article is part themed issue, "Understanding Link Between Environmental Pollutants, Brain & Behavior."

Language: Английский

Citations

1
Hippocampal GPR35 is involved in the depression-like behaviors induced by inflammation and mediates the antidepressant effects of fluoxetine in mice DOI

Kang Xu,

Zhi Xie, Yan Yang

et al.

Brain Behavior and Immunity, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 1, 2025

Language: Английский

Citations

1
Costunolide normalizes neuroinflammation and improves neurogenesis deficits in a mouse model of depression through inhibiting microglial Akt/mTOR/NF-κB pathway DOI Creative Commons

S. Zhang,

Qiao Deng,

Cheng Tian

et al.

Acta Pharmacologica Sinica, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 26, 2025

Abstract Neuroinflammation is crucial for the pathogenesis of major depression. Preclinical studies have shown potential anti-inflammatory agents, specifically costunolide (COS), correlate with antidepressant effects. In this study, we investigated molecular mechanisms underlying actions COS. Chronic restraint stress (CRS) was induced in male mice. The mice were treated either intra-DG injection COS (5 μM, 1 μL per side) or (20 mg/kg, i.p.) week. We showed that administration through both routes significantly ameliorated depressive-like behavior CRS-exposed Furthermore, improved chronic stress-induced adult hippocampal neurogenesis deficits attenuating microglia-derived neuroinflammation. demonstrated μM) exerted anti-neuroinflammatory effects LPS-treated BV2 cells via inhibiting microglial Akt/mTOR/NF-κB pathway; inactivation mTOR/NF-κB/IL-1β pathway required pro-neurogenic action Our results reveal mechanism normalizing neuroinflammation to improve deficits, supporting agents as a therapeutic strategy

Language: Английский

Citations

1
Activation of the CD200/CD200R1 axis improves cognitive impairment by enhancing hippocampal neurogenesis via suppression of M1 microglial polarization and neuroinflammation in hypoxic-ischemic neonatal rats DOI Creative Commons
Haitao Qian, Andi Chen,

Daoyi Lin

et al.

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 128, P. 111532 - 111532

Published: Jan. 21, 2024

Following hypoxic-ischemic brain damage (HIBD), there is a decline in cognitive function; however, are no effective treatment strategies for this condition neonates. This study aimed to evaluate the role of cluster differentiation 200 (CD200)/CD200R1 axis function following HIBD using an established model postnatal day 7 rats. Western blotting analysis was conducted protein expression levels CD200, CD200R1, proteins associated with PI3K/Akt-NF-κB pathway, and inflammatory factors such as TNF-α, IL-1β, IL-6 hippocampus. Additionally, double-immunofluorescence labeling utilized M1 microglial polarization neurogenesis To assess learning memory experimental rats, Morris water maze (MWM) test conducted. leads decrease CD200 CD200R1 neonatal rat hippocampus, while simultaneously increasing IL-6, IL-1β proteins, ultimately resulting impairment. The administration CD200Fc, fusion found enhance p-PI3K p-Akt, but reduce p-NF-κB. CD200Fc inhibited microglia, reduced neuroinflammation, improved hippocampal neurogenesis, mitigated impairment caused by In contrast, blocking interaction between anti-CD200R1 antibody (CD200R1 Ab) exerted opposite effect. Furthermore, PI3K specific activator, 740Y-P, significantly increased p-NF-κB expression. It also rats HIBD. Our findings illustrate that activation CD200/CD200R1 inhibits NF-κB-mediated microglia improve HIBD-induced disorder via PI3K/Akt signaling pathway.

Language: Английский

Citations

8
Traditional Pediatric Massage Enhanced Hippocampal GR, BDNF and IGF-1 Expressions and Exerted an Anti-depressant Effect in an Adolescent Rat Model of CUMS-induced Depression DOI
Rong Wu, Ying Xiong, Yun Gu

et al.

Neuroscience, Journal Year: 2024, Volume and Issue: 542, P. 47 - 58

Published: Feb. 15, 2024

Language: Английский

Citations

6