Parkinson hastalığında Glial hücre çaprazlaması: Mekanizmalar, çıkarımlar ve terapötik stratejiler.

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Parkinson's disease (PD) is a prevalent age-related neurodegenerative disorder marked by the progressive loss of dopaminergic neurons and the formation of Lewy bodies. Traditionally viewed as primarily a dopaminergic disorder, recent research has highlighted the significant role of neuroinflammation and the complex interplay between glial cells, particularly astrocytes and microglia, in PD pathogenesis. This review explores the multifaceted roles of astrocytes, microglia and oligodendrocytes in PD, focusing on their involvement in maintaining glutamate and ion homeostasis, energy metabolism, and the inflammatory response. We discuss the dual nature of these glial cells, which can both support and harm neuronal health under different conditions. We also examine the molecular mechanisms underlying glial cell communication, including cytokines, chemokines, extracellular vesicles, gap junctions, and neurotransmitter systems. Finally, we propose potential therapeutic strategies targeting these glial interactions to modulate neuroinflammation and protect neurons, offering new avenues for PD treatment. Understanding the diverse functions and interactions of glial cells in the central nervous system is crucial for developing effective interventions for PD and other neurodegenerative diseases.

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