International Immunopharmacology, Journal Year: 2024, Volume and Issue: 142, P. 113176 - 113176
Published: Sept. 20, 2024
Language: Английский
International Immunopharmacology, Journal Year: 2024, Volume and Issue: 142, P. 113176 - 113176
Published: Sept. 20, 2024
Language: Английский
Frontiers in Pharmacology, Journal Year: 2024, Volume and Issue: 15
Published: May 30, 2024
Traditionally, pharmacological mammalian/mechanistic targets of rapamycin (mTOR) kinase inhibitors have been used during transplantation and tumor treatment. Emerging pre-clinical evidence from the last decade displayed surprising effectiveness mTOR in ameliorating Alzheimer's Disease (AD), a common neurodegenerative disorder characterized by progressive cognitive function decline memory loss. Research shows activation as an early event AD development, inhibiting may promote resolution many hallmarks Alzheimer's. Aberrant protein aggregation, including amyloid-beta (Aβ) deposition tau filaments, defects, are reversed upon inhibition. A closer inspection highlighted temporal dependence hallmark-specific nature such beneficial effects. Time administration relative to disease progression, maintenance functional lysosomal system, could modulate its effectiveness. Moreover, inhibition also exerts distinct effects between neurons, glial cells, endothelial cells. Different properties produce different based on blood-brain barrier (BBB) entry capacities sites. This questions viable intervention strategy. In this review, we first summarize available their characteristics. We then comprehensively update discuss results resolve AD. Key pathologies discussed include Aβ deposition, tauopathies, aberrant neuroinflammation, neurovascular system breakdowns.
Language: Английский
Citations
5Experimental Eye Research, Journal Year: 2025, Volume and Issue: 251, P. 110235 - 110235
Published: Jan. 9, 2025
Language: Английский
Citations
0Frontiers in Cellular Neuroscience, Journal Year: 2025, Volume and Issue: 19
Published: April 7, 2025
Neuroinflammation is a fundamental feature of many chronic neurodegenerative diseases, where it contributes to disease onset, progression, and severity. This persistent inflammatory state arises from the activation innate adaptive immune responses within central nervous system (CNS), orchestrated by complex interplay resident cells, infiltrating peripheral an array molecular mediators such as cytokines, chemokines, extracellular vesicles. Among CNS-resident microglia play role, exhibiting dynamic spectrum phenotypes ranging neuroprotective neurotoxic. In sustained microglial often leads amplification cascades, reinforcing pathogenic cycle immune-mediated damage. Intercellular communication inflamed CNS persistence progression neuroinflammation. Microglia engage in extensive crosstalk with astrocytes, neurons, oligodendrocytes, shaping both local systemic responses. These interactions influence key processes synaptic pruning, phagocytosis, blood-brain barrier integrity, cytokine-mediated signaling. Understanding mechanisms cell-cell signaling this context critical for identifying therapeutic strategies modulate response restore homeostasis. review explores players neuroinflammation, focus on role microglia, pathways underlying intercellular communication, potential approaches mitigate neuroinflammatory damage diseases.
Language: Английский
Citations
0European Journal of Pharmacology, Journal Year: 2025, Volume and Issue: 990, P. 177269 - 177269
Published: Jan. 11, 2025
Language: Английский
Citations
0Aquaculture, Journal Year: 2023, Volume and Issue: 575, P. 739758 - 739758
Published: June 13, 2023
Language: Английский
Citations
8Journal of Nanobiotechnology, Journal Year: 2024, Volume and Issue: 22(1)
Published: Nov. 7, 2024
Abstract Optic nerve regeneration remains challenging worldwide due to the limited intrinsic regenerative capacity of retinal ganglion cells (RGCs) and inhibitory microenvironment. Oxidative stress, induced by excessive reactive oxygen species (ROS) following optic injury, is associated with prolonged neuroinflammation, resulting in a secondary injury RGCs impairment axon regeneration. Herein, we developed bionic nanocomposite scaffold (GA@PDA) immunoregulatory ability for enhanced The ice-templating method was employed fabricate biopolymer-based scaffolds directional porous structure, mimicking nerve, which effectively guided oriented growth neuronal cells. incorporation bioinspired polydopamine nanoparticles (PDA NPs) further confers excellent ROS scavenging ability, thereby modulating phenotype transformation microglia/macrophages from pro-inflammatory M1 anti-inflammatory M2. In rat crush model, implantation GA@PDA survival promoted axonal Our study offers novel insights holds promising potential advancement engineered biomaterials facilitating
Language: Английский
Citations
2Neuropharmacology, Journal Year: 2023, Volume and Issue: 242, P. 109746 - 109746
Published: Oct. 12, 2023
Language: Английский
Citations
5Molecular Aspects of Medicine, Journal Year: 2023, Volume and Issue: 94, P. 101219 - 101219
Published: Oct. 13, 2023
Language: Английский
Citations
5Cell Proliferation, Journal Year: 2024, Volume and Issue: 57(12)
Published: July 18, 2024
Traumatic optic neuropathy refers to nerve (ON) injury by trauma, including explosion and traffic accident. Retinal ganglion cell (RGC) death is the critical pathological cause of irreversible visual impairment blindness in ON injury. We previously investigated patterns 11 modes mouse retina post-ON Here we aimed identify additional signalling pathways regulating RGC survival rodents RNA sequencing analysis identified upregulation inflammation cellular senescence-related genes injury, which were confirmed immunoblotting immunofluorescence analyses. Increased expression senescence-associated β-galactosidase (SA-βgal) RGCs activation microglia also found. Transforming growth factor-β receptor type II inhibitor (LY2109761) treatment suppressed p15
Language: Английский
Citations
1Free Radical Biology and Medicine, Journal Year: 2023, Volume and Issue: 212, P. 415 - 432
Published: Dec. 20, 2023
Language: Английский
Citations
3