About this Research Topic
Insights of inflammation and degenerative diseases in the central nervous system (CNS) continue to evolve rapidly. Beyond cell-autonomous neuronal injury and death, light has been shed on multiple inflammatory properties of glia and invading leukocytes in most brain diseases. Novel knowledge has been fuelled by technological advancements such as cell type-specific transgenic animal models, live imaging techniques, single-cell next-generation sequencing, epigenetics, and genome-wide association studies, all enabled by novel bioinformatics and computational biology to drive an altered perspective on neurodegeneration and neuroinflammation. It is now reasonable to propose that the amelioration of chronic tissue damage and inflammation in, for example, amyotrophic lateral sclerosis, Huntington's disease, Parkinson's disease, Alzheimer's disease, frontotemporal lobar degeneration, traumatic brain injury and multiple sclerosis, will begin with an enhanced molecular understanding of the neuronal milieu and of its interaction with peripheral immune cells and mediators of inflammation.
Parenchymal and vascular players, as well as circulating leukocytes, have now been integrated into novel views of neurodegeneration. Astrocytes, CNS-resident microglia, barrier-associated macrophages, and antigen-presenting cells shape brain development, homeostasis, and regulate CNS pathologies in a bewildering diversity of ways. At the same time, the roles of meningeal and vascular inflammation and the further definition of immunosurveillance and leukocyte invasion through different brain barriers open new exciting frontiers of investigation on immune mechanisms in neurodegenerative disorders. To what extent is the infiltration of peripheral leukocytes, such as bone marrow-derived monocytes, neutrophils, B and T cells, ameliorative or propagative for CNS disorders? What roles do the various immune cell populations play in fostering disease onset, promoting chronic neuroinflammation or helping to defend against further injury? In this complex picture, intrinsic neurodegenerative mechanisms, also including glial activation and CNS barrier integrity, are shaped by genetic mutations and interact with CNS-extrinsic components such as circulating leukocytes, cytokines and growth factors, as well as environmental factors that predispose to CNS pathogenesis. Stressors include infections, inadequate nutrition, imbalanced gut microbiota, pollution, and adverse lifestyle.
In this Research Topic, we welcome authors to submit Original Research and Review articles focusing on but not limited to, the following subtopics:
1. Immune mechanisms uncovered in physiological model systems that shine new light on the role of inflammation on neuronal damage and repair in neurodegenerative diseases
2. Cell-cell interaction between neurons, glia and peripheral immune cells
3. Pre-clinical studies targeting the immune system mechanisms for emerging approaches to treat neurodegenerative diseases throughout the lifespan.
This collection intends to provide various perspectives on the protective and pathogenic aspects of neuroinflammatory processes to explore new possibilities and innovation for effective therapies against neurodegenerative diseases.
Topic Editor Prof. Gabriela Constantin is the co-founder of Leuvas Therapeutics. All other Topic Editors declare no competing interests with regards to the Research Topic subject.
Parenchymal and vascular players, as well as circulating leukocytes, have now been integrated into novel views of neurodegeneration. Astrocytes, CNS-resident microglia, barrier-associated macrophages, and antigen-presenting cells shape brain development, homeostasis, and regulate CNS pathologies in a bewildering diversity of ways. At the same time, the roles of meningeal and vascular inflammation and the further definition of immunosurveillance and leukocyte invasion through different brain barriers open new exciting frontiers of investigation on immune mechanisms in neurodegenerative disorders. To what extent is the infiltration of peripheral leukocytes, such as bone marrow-derived monocytes, neutrophils, B and T cells, ameliorative or propagative for CNS disorders? What roles do the various immune cell populations play in fostering disease onset, promoting chronic neuroinflammation or helping to defend against further injury? In this complex picture, intrinsic neurodegenerative mechanisms, also including glial activation and CNS barrier integrity, are shaped by genetic mutations and interact with CNS-extrinsic components such as circulating leukocytes, cytokines and growth factors, as well as environmental factors that predispose to CNS pathogenesis. Stressors include infections, inadequate nutrition, imbalanced gut microbiota, pollution, and adverse lifestyle.
In this Research Topic, we welcome authors to submit Original Research and Review articles focusing on but not limited to, the following subtopics:
1. Immune mechanisms uncovered in physiological model systems that shine new light on the role of inflammation on neuronal damage and repair in neurodegenerative diseases
2. Cell-cell interaction between neurons, glia and peripheral immune cells
3. Pre-clinical studies targeting the immune system mechanisms for emerging approaches to treat neurodegenerative diseases throughout the lifespan.
This collection intends to provide various perspectives on the protective and pathogenic aspects of neuroinflammatory processes to explore new possibilities and innovation for effective therapies against neurodegenerative diseases.
Topic Editor Prof. Gabriela Constantin is the co-founder of Leuvas Therapeutics. All other Topic Editors declare no competing interests with regards to the Research Topic subject.
Keywords: inflammation, neurodegeneration, astrocytes, microglia, myeloid cells, leukocyte trafficking
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.
