Molecular Neurobiology, Journal Year: 2025, Volume and Issue: unknown
Published: April 29, 2025
Language: Английский
Brain Disorders, Journal Year: 2025, Volume and Issue: unknown, P. 100210 - 100210
Published: March 1, 2025
Language: Английский
Citations
1
Journal of Affective Disorders Reports, Journal Year: 2024, Volume and Issue: 17, P. 100814 - 100814
Published: June 26, 2024
Post-traumatic stress disorder (PTSD) is a mental linked to neurochemical, hypothalamic-pituitary-adrenal (HPA)-axis dysregulations, inflammatory and pro-oxidant challenges in response traumatic events. It one of the leading causes neurocognitive declines, hence prompting need for pharmacological intervention. However, impact diosgenin, naturally occurring steroidal saponin with adaptogenic-like action, on PTSD-induced neuropsychiatric disturbances its underlying mechanisms are unknown. In this study, we investigated outcome diosgenin treatment multimodal traumatic, single prolonged (SPS)-induced PTSD mice. Following SPS-induced 7 days PTSD, mice (n = 9) were thereafter treated (25 50 mg/kg) or fluoxetine (10 orally from 8–20 (14 days). Locomotory, cognitive-, depressive- anxiety-like behaviors investigated. We assayed changes adrenal weight, serum glucose corticosterone concentrations. Neurochemical, inflammatory, oxido-nitrergic dysfunctions monoamine oxidase-B acetylcholinesterase activities, measured striatum, prefrontal-cortex hippocampus. The results revealed that SPS challenge inhibited locomotor, spatial/non-spatial memory functions, increased anxiety depressive-like features, which reversed by diosgenin. Diosgenin reduced oxidase-B, TNF-α, IL-6, malondialdehyde nitrite levels Antioxidants such as glutathione, superoxide-dismutase, catalase SPS-mice brains Moreover, attenuated hyper-HPA-axis mediation decreasing corticosterone, gland hypertrophy. Herewith, suggest convenes protection against exposed enhancing antioxidant machinery, neurochemical modulations, inhibition oxido-nitrergic, HPA-axis dysfunctions.
Language: Английский
Citations
7
Journal of Psychiatric Research, Journal Year: 2024, Volume and Issue: 179, P. 141 - 155
Published: Sept. 13, 2024
Language: Английский
Citations
7
Behavioural Brain Research, Journal Year: 2024, Volume and Issue: 480, P. 115397 - 115397
Published: Dec. 12, 2024
Language: Английский
Citations
5
Schizophrenia Bulletin, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 20, 2025
Relapsing after a first episode of schizophrenia (FES) is main predictor clinical and functional prognosis. Brain-derived neurotrophic factor (BDNF) plays critical role in neuronal development plasticity, its signaling may be altered by successive relapses. We assessed the impact relapse expression 2 isoforms BDNF tropomyosin-related kinase B (TrkB) receptor (active full-length TrkB-F inactive truncated TrkB-T) peripheral blood mononuclear cells from 53 FES patients remission followed up for 3 years. The group participants that relapsed (n = 24) during follow-up presented significant decrease active compared to baseline (M 100 ± 28.13 vs. M 83.42 33.84, t 2.5, P .02), with no changes TrkB-T nor plasma levels. This also led decline F/T ratio 1.13 0.38 0.94 0.36, 2.17, .041). No differences were found receptors' levels cases remained 29). These results not associated between groups terms pathway biomarkers, or treatment variables. findings highlight biological produces over systemic BDNF-TrkB pathway, potentially undermining crucial functions. Identifying actors involved can help design specific interventions prevention improve prognosis people early stages schizophrenia.
Language: Английский
Citations
0
Scientific Reports, Journal Year: 2025, Volume and Issue: 15(1)
Published: March 26, 2025
Cognitive impairment in schizophrenia occurs the early stages of disease and is closely associated with prognosis. Alleviation cognitive faces major challenges owing to lack preventive therapeutic drugs that are novel effective. Urolithin A (UA) a gut microbial metabolite ellagic acid has demonstrated neuroprotective effects multiple neurological models. Nonetheless, neuromodulatory role UA yet be elucidated. Wistar rat pups were separated from their mothers for 24 h on postnatal days (PNDs) 9–10 establish an early-life stress model. The pretreated at different administration times (2, 4, 6 weeks) doses (50, 100, 150 mg/kg) adolescence (PND29). Behavioral tests performed after end administration. Subsequently, hippocampal samples collected histopathological molecular evaluations. Male offspring rats subjected maternal separation exhibited increased sensitivity prepulse inhibition impairment, accompanied by severe neuroinflammation impaired neurogenesis. However, attenuated separation-induced deficits impairments restored neurogenesis dose-dependent manner. Furthermore, pretreatment preserved dendritic spine density, synapses, presynaptic vesicles. In addition, it exerted anti-inflammatory inhibiting microglial activation expression proinflammatory cytokines tumor necrosis factor-α, interleukin-6, interleukin-1β. Potential mechanisms included upregulation brain-derived neurotrophic factor protein extracellular signal-regulated kinase signaling pathway. This study first preclinical evaluation schizophrenia. findings suggest changes function linked driven interaction among neuroinflammation, neurogenesis, synaptic plasticity potential reverse these processes. These observations provide evidence future clinical trials as dietary supplement preventing
Language: Английский
Citations
0
Molecular Neurobiology, Journal Year: 2025, Volume and Issue: unknown
Published: April 9, 2025
Language: Английский
Citations
0
Molecular Neurobiology, Journal Year: 2025, Volume and Issue: unknown
Published: April 29, 2025
Language: Английский
Citations
0