
Immunity, Journal Year: 2023, Volume and Issue: 56(9), P. 1983 - 1985
Published: Sept. 1, 2023
Language: Английский
Immunity, Journal Year: 2023, Volume and Issue: 56(9), P. 1983 - 1985
Published: Sept. 1, 2023
Language: Английский
BMC Medicine, Journal Year: 2024, Volume and Issue: 22(1)
Published: Oct. 8, 2024
Individuals who have experienced severe traumatic events are estimated to a post-traumatic stress disorder (PTSD) prevalence rate ranging from 10 50%, while those not affected by trauma exposure often considered possess psychological resilience. However, the neural mechanisms underlying development of PTSD, especially resilience after trauma, remain unclear. This study aims investigate changes cortical morphometric similarity network (MSN) in PTSD and trauma-exposed healthy individuals (TEHI), as well associated molecular alterations gene expression, providing potential targets for prevention intervention PTSD.
Language: Английский
Citations
2International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(20), P. 11245 - 11245
Published: Oct. 19, 2024
Mood disorders mainly affect the patient's daily life, lead to suffering and disability, increase incidence rate of many medical illnesses, even cause a trend suicide. The glucocorticoid (GC)-mediated hypothalamus-pituitary-adrenal (HPA) negative feedback regulation plays key role in neuropsychiatric disorders. balance mineralocorticoid receptor (MR)/glucocorticoid (GR) level contributes maintaining homeostasis neuroendocrine system. Consistently, chronic excess GC can also HPA axis dysfunction, triggering anxiety, depression, memory loss, cognitive impairment. animal model induced by corticosterone (CORT) administration has been widely adopted because its simple replication strong stability. This review summarizes behavioral changes underlying mechanisms CORT administration-induced models, including neuroinflammatory response, pyroptosis, oxidative stress, neuroplasticity, apoptosis. Notably, at different doses cycles destroy MR/GR ratio make dose-dependent effects on central nervous system (CNS). work aims offer an overview topic recommendations for future function research.
Language: Английский
Citations
2Journal of Neurochemistry, Journal Year: 2024, Volume and Issue: 169(1)
Published: Dec. 16, 2024
Abstract Neuron–glia interactions are fundamental to the development and function of nervous system. During development, glia, including astrocytes, microglia, oligodendrocytes, influence neuronal differentiation migration, synapse formation refinement, myelination. In mature brain, glia crucial for maintaining neural homeostasis, modulating synaptic activity, supporting metabolic functions. Neurons, inherently vulnerable various stressors, rely on protection repair. However, in their reactive state, can also promote damage, which contributes neurodegenerative neuropsychiatric diseases. Understanding dual role glia—as both protectors potential aggressors—sheds light complex contributions disease etiology pathology. By appropriately glial it may be possible mitigate neurodegeneration restore function. this review, originated from International Society Neurochemistry (ISN) Advanced School 2019 held Montreal, Canada, we first describe critical importance maintenance a healthy system as well damage neurological disorders. We then discuss strategies modulate activity during protect properly functioning propose that targeting cells presents promising therapeutic avenue rebuilding image
Language: Английский
Citations
2bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown
Published: July 5, 2024
Abstract Astrocytes participate in the clearance of obsolete or unwanted neuronal synapses. However, molecular machinery recruited for recognition synapses is not fully clarified, especially pathological conditions. Here, we investigated phagocytic process through individual gene silencing using a druggable library. Our study demonstrates that astrocyte-mediated synapse engulfment regulated by Atypical chemokine receptor 3 (Ackr3). Mechanistically, have shown Ackr3 recognizes phosphatidylethanolamine (PE)-bound Cxcl12 at synaptic terminals both vitro and cell culture thus serving as novel marker dysfunction. Notably, its ligand are overexpressed post-mortem AD human brains, downregulation mouse models (5xFAD) significantly diminishes elimination. Overall, this work unveils novel, possibly targetable mechanism implicated most common neurodegenerative disease.
Language: Английский
Citations
1Immunity, Journal Year: 2023, Volume and Issue: 56(9), P. 1983 - 1985
Published: Sept. 1, 2023
Language: Английский
Citations
2