Journal of Oral Biosciences, Journal Year: 2024, Volume and Issue: unknown, P. 100596 - 100596
Published: Dec. 1, 2024
Language: Английский
Journal of Oral Biosciences, Journal Year: 2024, Volume and Issue: unknown, P. 100596 - 100596
Published: Dec. 1, 2024
Language: Английский
Nature Communications, Journal Year: 2024, Volume and Issue: 15(1)
Published: Feb. 21, 2024
Astrocytes express ionotropic receptors, including N-methyl-D-aspartate receptors (NMDARs). However, the contribution of NMDARs to astrocyte-neuron interactions, particularly in vivo, has not been elucidated. Here we show that a knockdown approach selectively reduce mouse cortical astrocytes decreases astrocyte Ca
Language: Английский
Citations
12Molecular Neurodegeneration, Journal Year: 2025, Volume and Issue: 20(1)
Published: March 31, 2025
Abstract Immune mechanisms play a fundamental role in Alzheimer’s disease (AD) pathogenesis, suggesting that approaches which target immune cells and immunologically relevant molecules can offer therapeutic opportunities beyond the recently approved amyloid beta monoclonal therapies. In this review, we provide an overview of immunomodulatory therapeutics development, including their preclinical evidence clinical trial results. Along with detailing processes involved AD pathogenesis highlighting how these be therapeutically targeted to modify progression, summarize knowledge gained from previous trials immune-based interventions, series recommendations for development future treat AD.
Language: Английский
Citations
2Trends in Cell Biology, Journal Year: 2024, Volume and Issue: unknown
Published: June 1, 2024
Language: Английский
Citations
8The American Journal of Human Genetics, Journal Year: 2024, Volume and Issue: 111(4), P. 729 - 741
Published: April 1, 2024
Language: Английский
Citations
5Neuroscience, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 1, 2025
Language: Английский
Citations
0Exploration of neuroscience, Journal Year: 2025, Volume and Issue: unknown
Published: March 11, 2025
Purinergic signaling, mediated by ATP and adenosine receptors, plays a crucial role in cellular communication homeostasis within the central nervous system (CNS), particularly regulating synaptic activity, glial cell functions, neuroplasticity. Glial cells, including astrocytes microglia, contribute to both short-term processes, such as neurotransmission neuroinflammation, long-term remodeling, tissue repair, behavioral adaptation. Dysregulation of purinergic signaling these cells has been implicated pathogenesis various neurodegenerative neuropsychiatric disorders. This article explores evolving concept synapse, highlighting active modulation emphasizing significance function responses conditions injury neurotoxicity. Specifically, it examines roles receptors—such P2X4, P2X7, P2Y1, P2Y12—in mediating key astrocytic microglial phagocytosis, plasticity, neuronal damage. Furthermore, discusses involvement receptors neurological disorders epilepsy, Alzheimer’s disease, Parkinson’s multiple sclerosis, ischemic stroke, Rett syndrome, autism spectrum disorder, well potential therapeutic strategies targeting mitigate inflammation, promote improve clinical outcomes.
Language: Английский
Citations
0MedComm, Journal Year: 2025, Volume and Issue: 6(5)
Published: April 17, 2025
ABSTRACT The gliotransmitter adenosine 5'‐triphosphate (ATP) and its enzymatic degradation product play a major role in orchestrating the hippocampus cognitive affective functions via P2 purinoceptors (P2X, P2Y) P1 receptors (A1, A2A). Although numerous reviews exist on that modulate these functions, there is an apparent gap relating to involvement of astrocyte‐derived extracellular ATP. Our review focuses following issues: An impeded release ATP from hippocampal astrocytes through vesicular mechanisms or connexin hemichannels pannexin channels interferes with spatial working memory rodents. pharmacological blockade P2Y1 (P2Y1Rs) reverses deficits learning/memory performance mouse models familial Alzheimer's disease (AD). Similarly, depressive disorder (MDD), based acute chronic stress‐induced development depressive‐like behavior, reduced exocytotic/channel‐mediated results deterioration behavioral responses. However, opposite, increased stimulation microglial/astrocytic P2X7R‐channel by causes neuroinflammation consequence behavior. In conclusion, strong evidence for assumption intimately involved pathophysiology neuron/astrocyte‐based human illnesses opening new diagnostic therapeutic vistas AD MDD.
Language: Английский
Citations
0Biomedicines, Journal Year: 2025, Volume and Issue: 13(5), P. 1121 - 1121
Published: May 6, 2025
Stress and sleep share a reciprocal relationship, where chronic stress often leads to disturbances that worsen neurodegenerative psychiatric conditions. Non-neuronal cells, particularly astrocytes microglia, play critical roles in the brain’s response regulation of sleep. Astrocytes influence architecture by regulating adenosine signaling glymphatic clearance, both which can be disrupted stress, leading reduced restorative Microglia, activated under conditions, drive neuroinflammatory processes further impair exacerbate brain dysfunction. Additionally, gut–brain axis mediates interactions between sleep, inflammation, with microbial metabolites influencing neural pathways. Many these effects converge on disruption synaptic processes, such as neurotransmitter balance, plasticity, pruning, turn contribute pathophysiology disorders. This review explores how cellular systemic mechanisms stress-induced their implications for disorders, offering insights into potential therapeutic strategies targeting non-neuronal cells axis.
Language: Английский
Citations
0Cell Reports, Journal Year: 2025, Volume and Issue: 44(6), P. 115765 - 115765
Published: May 28, 2025
Language: Английский
Citations
0bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown
Published: Oct. 24, 2024
Updating behavior based on feedback from the environment is a crucial means by which organisms learn and develop optimal behavioral strategies
Language: Английский
Citations
2