
European Journal of Pharmacology, Год журнала: 2025, Номер unknown, С. 177422 - 177422
Опубликована: Фев. 1, 2025
Язык: Английский
European Journal of Pharmacology, Год журнала: 2025, Номер unknown, С. 177422 - 177422
Опубликована: Фев. 1, 2025
Язык: Английский
Brain Behavior and Immunity, Год журнала: 2023, Номер 115, С. 64 - 79
Опубликована: Окт. 2, 2023
Язык: Английский
Процитировано
21Journal of Affective Disorders, Год журнала: 2023, Номер 334, С. 278 - 292
Опубликована: Май 6, 2023
Язык: Английский
Процитировано
19Trends in Neurosciences, Год журнала: 2024, Номер 47(11), С. 933 - 948
Опубликована: Сен. 21, 2024
Язык: Английский
Процитировано
7Theranostics, Год журнала: 2024, Номер 14(10), С. 4058 - 4075
Опубликована: Янв. 1, 2024
Knowledge about the pathogenesis of depression and treatments for this disease are lacking. Epigenetics-related circRNAs likely involved in mechanism have great potential as treatment targets, but their action is still unclear.
Язык: Английский
Процитировано
6Biomedicine & Pharmacotherapy, Год журнала: 2023, Номер 163, С. 114852 - 114852
Опубликована: Май 8, 2023
Major depressive disorder (MDD) is a prominent psychiatric with high prevalence rate. The recent COVID-19 pandemic has exacerbated the already of MDD. Unfortunately, significant proportion patients are unresponsive to conventional treatments, necessitating exploration novel therapeutic strategies. Oxytocin, an endogenous neuropeptide, emerged as promising candidate anxiolytic and antidepressant properties. Oxytocin been shown alleviate emotional disorders by modulating hypothalamic-pituitary-adrenal (HPA) axis central immune system. dysfunction system strongly linked onset progression depression. believed be key target oxytocin in ameliorating disorders. In this review, we examine evidence regarding interactions between oxytocin, system, disorder. Moreover, summarize speculate on potential roles intertwined association treating
Язык: Английский
Процитировано
16Gut Microbes, Год журнала: 2024, Номер 16(1)
Опубликована: Март 15, 2024
The gut microbiota exerts a mutualistic interaction with the host in fragile ecosystem and intestinal, neural, immune cells. Perturbations of gastrointestinal track composition after stress have profound consequences on central nervous system system. Reciprocally, brain signals affect highlighting bidirectional communication between gut. Here, we focus potential role inflammation mediating stress-induced gut-brain changes discuss impact several cells inflammatory molecules dialogue stress. Understanding microbial might provide new avenues for therapy.
Язык: Английский
Процитировано
5Life, Год журнала: 2024, Номер 14(5), С. 578 - 578
Опубликована: Апрель 30, 2024
Investigating the biophysiological substrates of psychiatric illnesses is great interest to our understanding disorders’ etiology, identification reliable biomarkers, and potential new therapeutic avenues. Schizophrenia represents a consolidated model γ alterations arising from aberrant activity parvalbumin-positive GABAergic interneurons, whose dysfunction associated with perineuronal net impairment neuroinflammation. This pathogenesis supported by molecular, cellular, functional evidence. Proof for oscillations their underlying mechanisms has also been reported in bipolar disorder an emerging topic major depressive disorder. Although evidence animal models needs be further elucidated humans, pathophysiology γ-band alteration common denominator different neuropsychiatric disorders. The purpose this narrative review outline framework converging results conditions characterized abnormality, neurochemical brain rhythms.
Язык: Английский
Процитировано
5Diabetology & Metabolic Syndrome, Год журнала: 2023, Номер 15(1)
Опубликована: Авг. 31, 2023
Abstract Type 2 diabetes (T2D) is a metabolic disease caused by the development of insulin resistance (IR), relative deficiency, and hyperglycemia. Hyperglycemia-induced neurochemical dysregulation activates progression depression in T2D patients. Therefore, management antidepressant agents improves glucose homeostasis sensitivity. However, prolong use drugs may increase risk for T2D. there strong controversy concerning this review try to elucidate potential effects regarding their detrimental beneficial effects.
Язык: Английский
Процитировано
12International Immunopharmacology, Год журнала: 2024, Номер 143, С. 113367 - 113367
Опубликована: Окт. 16, 2024
Язык: Английский
Процитировано
4Cells, Год журнала: 2024, Номер 13(21), С. 1791 - 1791
Опубликована: Окт. 29, 2024
Major Depressive Disorder (MDD) is a prevalent mental health condition with complex pathophysiology involving neuroinflammation, neurodegeneration, and disruptions in neuronal glial cell function. Microglia, the innate immune cells of central nervous system, release inflammatory cytokines response to pathological changes associated MDD. Damage-associated molecular patterns (DAMPs) act as alarms, triggering microglial activation subsequent cytokine release. This review examines cellular mechanisms underlying MDD pathophysiology, focusing on lipid-mediated modulation neuroinflammation. We explore intricate roles microglia astrocytes propagating cascades discuss how these processes affect integrity at level. Central our analysis are three key molecules: High Mobility Group Box 1 (HMGB1) S100 Calcium Binding Protein β (S100β) alarmins, Neuron-Specific Enolase (NSE) an indicator stress. present evidence from vitro ex vivo studies demonstrating molecules reflect contribute neuroinflammatory milieu characteristic The then explores potential omega-3 polyunsaturated fatty acids (ω-3 PUFAs) neuroinflammation modulators, examining their effects activation, production, resilience models depression. critically analyze experimental data ω-3 PUFA supplementation influences expression HMGB1, S100β, NSE cultures. By integrating findings lipidomic neurobiology, this aims elucidate by which PUFAs may exert antidepressant through markers. These insights understanding neuroprotection inform development targeted, lipid-based therapies for both depression neurodegenerative disorders.
Язык: Английский
Процитировано
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