Research studies in neurodegenerative diseases have traditionally focused on the investigation of neuronal dysfunction, while little attention has been brought to the role of glial cells of the CNS or PNS. However, over the last decade, it has become widely accepted that microglia and macroglia (astrocytes, oligodendrocytes) greatly contribute to the degeneration of neurons observed in a variety of neurodegenerative diseases. The contribution of these cell types and the presence of potential non-cell autonomous mechanisms of disease pathogenesis are now extensively being studied using diverse disease model systems. These studies have highlighted a complex regulation between neuron and glia, but also glia and glia, suggesting that any dysfunction among these cellular cross talks contributes to neuronal cell death.
While it is agreed upon that glial cells contribute to neuronal death in neurodegenerative diseases, the precise mechanisms for this contribution and the presence of disease-specific pathways is still unknown. Therefore, the goal of this research topic is to present new data on glia-neuron and/or glia-glia crosstalk in varying neurodegenerative diseases. The use of state-of-the-art model system and technologies will be highlighted and could include single nuclei RNA sequencing, human iPSC model systems (2D, 3D), brain organoid studies, spatial transcriptomics analyses and/or innovative proteomics analyses. In addition, comprehensive review articles summarizing the most recent findings and discoveries on glial regulation of neuronal degenerations will provide important background information and is greatly welcomed as a contribution to this research topic.
The present article collection should cover, but is not limited to, studies on:
• Research articles and review articles
• Glia-neuron interaction
• Glia-glia interaction
• Innovative model systems to study the contribution of glia to neurodegeneration, including human cell models and complex in vivo studies
• Innovative technologies to study glial dysfunction
Research studies in neurodegenerative diseases have traditionally focused on the investigation of neuronal dysfunction, while little attention has been brought to the role of glial cells of the CNS or PNS. However, over the last decade, it has become widely accepted that microglia and macroglia (astrocytes, oligodendrocytes) greatly contribute to the degeneration of neurons observed in a variety of neurodegenerative diseases. The contribution of these cell types and the presence of potential non-cell autonomous mechanisms of disease pathogenesis are now extensively being studied using diverse disease model systems. These studies have highlighted a complex regulation between neuron and glia, but also glia and glia, suggesting that any dysfunction among these cellular cross talks contributes to neuronal cell death.
While it is agreed upon that glial cells contribute to neuronal death in neurodegenerative diseases, the precise mechanisms for this contribution and the presence of disease-specific pathways is still unknown. Therefore, the goal of this research topic is to present new data on glia-neuron and/or glia-glia crosstalk in varying neurodegenerative diseases. The use of state-of-the-art model system and technologies will be highlighted and could include single nuclei RNA sequencing, human iPSC model systems (2D, 3D), brain organoid studies, spatial transcriptomics analyses and/or innovative proteomics analyses. In addition, comprehensive review articles summarizing the most recent findings and discoveries on glial regulation of neuronal degenerations will provide important background information and is greatly welcomed as a contribution to this research topic.
The present article collection should cover, but is not limited to, studies on:
• Research articles and review articles
• Glia-neuron interaction
• Glia-glia interaction
• Innovative model systems to study the contribution of glia to neurodegeneration, including human cell models and complex in vivo studies
• Innovative technologies to study glial dysfunction