The majority of human diseases that affect the central nervous system (CNS) involve not only dysfunction and/or death of neuronal cells, but also contributions from non-neuronal cells known as glia. Glia performs essential functions to maintain brain homeostasis and exist in roughly equal numbers as neurons in the human brain, with some regional variability. While much research over the past century has focused on how neurons and neural circuits are affected in various disease states until recently, much less attention was paid to determining roles for glia in neuropathological conditions. However, an explosion of new information has pointed to central and complex roles for glia in the pathogenesis of neurological disorders.
Most neurological diseases occur sporadically and with unknown etiology, but much evidence suggests that the underlying pathogenic events are similar. For example, a shared molecular feature of all neurodegenerative diseases, such as Alzheimer, Parkinson, and Huntington diseases, is the accumulation of toxic protein aggregates that result from disrupted proteostasis in cells. Remarkably, one of the most prominent and earliest features observed in neurodegenerative disease patient brains is the appearance of reactive astrocytes and microglia in areas of the brain experiencing neuronal cell loss. Reactive glial proliferate and migrate to these brain regions to clear debris and dying neurons and promote neuronal recovery and regrowth. However, persistent, uncontrolled glial cell activation leads to a neuroinflammatory state that drives disease progression. As we expand our understanding of the specific molecular pathways involved in neuropathogenesis, it is becoming increasingly clear that glia plays active roles in these processes. For example, activated glia can directly contribute to synapse loss, cross-activation of other glial cell types, and promote the prion-like spreading of pathogenic protein aggregates in the brain. In addition, a growing number of glial genes have been identified in genome-wide association studies of many neurological disorders, highlighting the importance of non-neuronal cell types in disease.
There is a growing body of evidence suggesting that glia plays both beneficial and detrimental roles in neurological disease states. Gaining a better understanding of the pathways involved in the numerous glial responses to neuronal injury or insult is crucial for exploring new potential therapeutic avenues for these diseases, many of which remain incurable. This special issue, “Glial Cells as an Emerging Therapeutic Target in the Pathobiology of Central Nervous System Disorders: Friend or Foe?” will explore the seemingly-“double-edged” roles that oligodendrocytes, microglia, astrocytes, and ependymal cells play in the wide-ranging of CNS disorders. The manuscripts included in this issue will help to inspire new thinking about the similarities and differences between reactive glia in various disease settings and lend insight into ways that non-neuronal cells could be targeted therapeutically. The special issue seeks to publish novel research and reflect the most recent advances on the latest contributions on the above areas, covering new signaling pathways and therapeutic targets, as well as innovative review articles. This Special Issue should be of benefit to researchers worldwide, wherever there is a need to overcome challenges, design therapeutic options, and strive for novel drug breakthroughs towards a new era of glia-neuron interactions in CNS disorders.
We invite contributions on the following disorders including but not limited to:
• Alzheimer
• Parkinson
• Huntington
• Multiple sclerosis
• Amyotrophic lateral sclerosis
• Neuropsychiatric disorders
• Neurodevelopmental disorder
The majority of human diseases that affect the central nervous system (CNS) involve not only dysfunction and/or death of neuronal cells, but also contributions from non-neuronal cells known as glia. Glia performs essential functions to maintain brain homeostasis and exist in roughly equal numbers as neurons in the human brain, with some regional variability. While much research over the past century has focused on how neurons and neural circuits are affected in various disease states until recently, much less attention was paid to determining roles for glia in neuropathological conditions. However, an explosion of new information has pointed to central and complex roles for glia in the pathogenesis of neurological disorders.
Most neurological diseases occur sporadically and with unknown etiology, but much evidence suggests that the underlying pathogenic events are similar. For example, a shared molecular feature of all neurodegenerative diseases, such as Alzheimer, Parkinson, and Huntington diseases, is the accumulation of toxic protein aggregates that result from disrupted proteostasis in cells. Remarkably, one of the most prominent and earliest features observed in neurodegenerative disease patient brains is the appearance of reactive astrocytes and microglia in areas of the brain experiencing neuronal cell loss. Reactive glial proliferate and migrate to these brain regions to clear debris and dying neurons and promote neuronal recovery and regrowth. However, persistent, uncontrolled glial cell activation leads to a neuroinflammatory state that drives disease progression. As we expand our understanding of the specific molecular pathways involved in neuropathogenesis, it is becoming increasingly clear that glia plays active roles in these processes. For example, activated glia can directly contribute to synapse loss, cross-activation of other glial cell types, and promote the prion-like spreading of pathogenic protein aggregates in the brain. In addition, a growing number of glial genes have been identified in genome-wide association studies of many neurological disorders, highlighting the importance of non-neuronal cell types in disease.
There is a growing body of evidence suggesting that glia plays both beneficial and detrimental roles in neurological disease states. Gaining a better understanding of the pathways involved in the numerous glial responses to neuronal injury or insult is crucial for exploring new potential therapeutic avenues for these diseases, many of which remain incurable. This special issue, “Glial Cells as an Emerging Therapeutic Target in the Pathobiology of Central Nervous System Disorders: Friend or Foe?” will explore the seemingly-“double-edged” roles that oligodendrocytes, microglia, astrocytes, and ependymal cells play in the wide-ranging of CNS disorders. The manuscripts included in this issue will help to inspire new thinking about the similarities and differences between reactive glia in various disease settings and lend insight into ways that non-neuronal cells could be targeted therapeutically. The special issue seeks to publish novel research and reflect the most recent advances on the latest contributions on the above areas, covering new signaling pathways and therapeutic targets, as well as innovative review articles. This Special Issue should be of benefit to researchers worldwide, wherever there is a need to overcome challenges, design therapeutic options, and strive for novel drug breakthroughs towards a new era of glia-neuron interactions in CNS disorders.
We invite contributions on the following disorders including but not limited to:
• Alzheimer
• Parkinson
• Huntington
• Multiple sclerosis
• Amyotrophic lateral sclerosis
• Neuropsychiatric disorders
• Neurodevelopmental disorder