Research Topic

Neuroglia in Neuropsychiatric Disorders

About this Research Topic

Neuropsychiatric disorders such as major depression, anxiety, bipolar disorder, schizophrenia and post-traumatic stress disorder affect millions of people worldwide with a consistent impact on social and healthcare costs. These disorders are usually characterized by a progressive loss of cognitive and functional abilities which result in aberrant behavior and lead to debility and early death. The pathophysiological mechanisms underlying mental illness are still unknown which hamper the development of better therapeutic strategies. Recently, glial cell dysregulation has been highlighted in many pathophysiological aspects of neuropsychiatric disorders. Glia, also known as glial cells, are non-neuronal cells which comprise a vast fraction of the cell population in the mammalian brain. Glial cells comprise astrocytes, oligodendrocytes, and microglia which provide support for neuronal function and are, thus, essential in normal brain activity. Therefore, glial cells present an attractive target for increasing our understanding of mental illness and developing novel therapeutic strategies.

Glial cells are highly heterogeneous, providing a plethora of supporting functions which are important for normal brain activity. The majority of these aspects can be detrimentally affected in neuropsychiatric disorders leading to a cascade of events which can lead to aberrant behaviors, disabilities and cognitive decline. In this Research Topic, we aim to provide evidence of the importance of glial cells in mental illness and shift our view from “passengers on the back seat” to major contributors and possible therapeutic targets in cognitive disorders. We, therefore, welcome contributions that target, but are not limited to, the following themes:

- Factors regulating neuron-glia communications
- Mechanisms regulating inflammation, gliosis
- Perturbation of signaling pathway involved in behavioral changes
- Novel phenomena of cell-to-cell communication
- Novel signals driving White matter loss, myelination, remyelination
- Synthetic or natural compounds acting on glia
- Molecular consequence of the physical interaction with neurons, glial cells, extracellular matrix, cerebral vessels, components of the blood-brain barrier
- Extracellular environments
- Signals regulating cell-fate
- Factors influencing CNS development, neurogenesis and metabolism
- Risk factors contributing to spatial heterogeneity and heterochronicity

To note, Dr. Rivera and Prof. Butt are both shareholders and founders of Gliagenesis LTD. The other Topic Editors have no other competing interests to declare


Keywords: Glia, Astrocytes, Oligodendrocytes, Microglia, Schizophrenia, Bipolar Disorder, Mood Disorders


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

Neuropsychiatric disorders such as major depression, anxiety, bipolar disorder, schizophrenia and post-traumatic stress disorder affect millions of people worldwide with a consistent impact on social and healthcare costs. These disorders are usually characterized by a progressive loss of cognitive and functional abilities which result in aberrant behavior and lead to debility and early death. The pathophysiological mechanisms underlying mental illness are still unknown which hamper the development of better therapeutic strategies. Recently, glial cell dysregulation has been highlighted in many pathophysiological aspects of neuropsychiatric disorders. Glia, also known as glial cells, are non-neuronal cells which comprise a vast fraction of the cell population in the mammalian brain. Glial cells comprise astrocytes, oligodendrocytes, and microglia which provide support for neuronal function and are, thus, essential in normal brain activity. Therefore, glial cells present an attractive target for increasing our understanding of mental illness and developing novel therapeutic strategies.

Glial cells are highly heterogeneous, providing a plethora of supporting functions which are important for normal brain activity. The majority of these aspects can be detrimentally affected in neuropsychiatric disorders leading to a cascade of events which can lead to aberrant behaviors, disabilities and cognitive decline. In this Research Topic, we aim to provide evidence of the importance of glial cells in mental illness and shift our view from “passengers on the back seat” to major contributors and possible therapeutic targets in cognitive disorders. We, therefore, welcome contributions that target, but are not limited to, the following themes:

- Factors regulating neuron-glia communications
- Mechanisms regulating inflammation, gliosis
- Perturbation of signaling pathway involved in behavioral changes
- Novel phenomena of cell-to-cell communication
- Novel signals driving White matter loss, myelination, remyelination
- Synthetic or natural compounds acting on glia
- Molecular consequence of the physical interaction with neurons, glial cells, extracellular matrix, cerebral vessels, components of the blood-brain barrier
- Extracellular environments
- Signals regulating cell-fate
- Factors influencing CNS development, neurogenesis and metabolism
- Risk factors contributing to spatial heterogeneity and heterochronicity

To note, Dr. Rivera and Prof. Butt are both shareholders and founders of Gliagenesis LTD. The other Topic Editors have no other competing interests to declare


Keywords: Glia, Astrocytes, Oligodendrocytes, Microglia, Schizophrenia, Bipolar Disorder, Mood Disorders


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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Submission Deadlines

31 October 2021 Abstract
31 January 2022 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

31 October 2021 Abstract
31 January 2022 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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