About this Research Topic
The central nervous system (CNS) and the immune system are deeply interconnected, capable of dynamic surveillance. This Research Topic aims to explore the cellular and molecular foundations of neuro-immune communication, focusing on how the interplay influences neurodegenerative diseases such as Alzheimer’s Disease (AD) and conditions following traumatic brain injury (TBI) or microbiota.
Neuro-immune crosstalk can manifest in various forms, from brain-originated substances entering the blood to direct infiltration of peripheral immune cells into brain parenchyma. Resident immune cells like microglia are crucial for maintaining homeostasis and responding to injury or disease through phagocytosis and modulation of immune responses. In the context of neurodegenerative diseases, both innate and adaptive immune responses are critical in the disease's initiation and progression. For instance, AD is marked by extracellular amyloid-β (Aβ) deposition and intracellular hyperphosphorylated tau aggregation, which, along with immune responses, drive neuronal loss and cognitive decline. Additional factors influencing AD include Circadian rhythm, TBI and gut microbiota, which affect systemic inflammation and neurodegeneration progression.
Recent studies highlight the significant role of gut microbiota in both the development and progression of AD. The gut-brain axis is identified as a crucial pathway, with changes in gut microbiota composition affecting CNS function and potentially triggering neuroinflammatory responses. Specific gut-derived metabolites, like short-chain fatty acids (SCFAs), have shown anti-inflammatory properties and could enhance the integrity of the blood-brain barrier, offering potential neuroprotection. Surgical stress and conditions like postoperative delirium further underscore the importance of gut microbiota in systemic inflammation and cognitive impairments.
In the realm of TBI, neuroinflammation is a dynamic process involving both peripheral and central immune cells, evolving over time and influencing injury severity and recovery. Hypoxemia post-injury exacerbates neuroinflammation and chronic cognitive deficits, although the exact mechanisms remain unclear. Gut microbiota modulation has emerged as a significant factor in TBI recovery, with changes in gut microbiome composition impacting neuroinflammation, neurogenesis, and long-term outcomes. Interactions between immune cells and gut metabolites, as well as the role of specific T cell subsets, are areas of active investigation.
Moreover, the interorgan connection during critical illness, such as acute kidney injury (AKI), reveals significant insights into CNS inflammation and behaviour changes. Identifying drivers of brain inflammation post-AKI, whether mediated by peripheral immune cells, kidney molecular mediators, or systemic inflammation, is vital for understanding cognitive dysfunction and developing therapeutic strategies.
This Research Topic invites contributions that review current progress and explore innovative angles on immune regulation in AD and TBI. This includes examining roles of microglia, cytokines, and other neuroinflammation axis, and leveraging advanced technologies like single-cell RNA sequencing and imaging to uncover novel regulatory pathways. Manuscripts that elucidate the interplay between systemic and CNS immune responses and propose potential therapeutic targets to modulate immune activity are particularly welcome. By fostering a deeper understanding of these complex neuro-immune interactions, we aim to pave the way for innovative treatments to slow or halt disease progression and improve recovery outcomes.
This Research Topic, seeks Original Research, Review, Mini-Review, Hypothesis and Theory, Perspective, Clinical Trial, Case Report, and Opinion articles that cover, but are not limited to, the following topics:
1. Brain-immune interactions in AD
2. Genetic and epigenetic regulation in microglia in AD
3. Barrier systems
4. Gut-brain interactions
5. Circadian rhythm and Sleep
6. Genetic risk factors and GWAS study
7. New technology in neuroinflammation and studies in AD
Neuro-immune crosstalk can manifest in various forms, from brain-originated substances entering the blood to direct infiltration of peripheral immune cells into brain parenchyma. Resident immune cells like microglia are crucial for maintaining homeostasis and responding to injury or disease through phagocytosis and modulation of immune responses. In the context of neurodegenerative diseases, both innate and adaptive immune responses are critical in the disease's initiation and progression. For instance, AD is marked by extracellular amyloid-β (Aβ) deposition and intracellular hyperphosphorylated tau aggregation, which, along with immune responses, drive neuronal loss and cognitive decline. Additional factors influencing AD include Circadian rhythm, TBI and gut microbiota, which affect systemic inflammation and neurodegeneration progression.
Recent studies highlight the significant role of gut microbiota in both the development and progression of AD. The gut-brain axis is identified as a crucial pathway, with changes in gut microbiota composition affecting CNS function and potentially triggering neuroinflammatory responses. Specific gut-derived metabolites, like short-chain fatty acids (SCFAs), have shown anti-inflammatory properties and could enhance the integrity of the blood-brain barrier, offering potential neuroprotection. Surgical stress and conditions like postoperative delirium further underscore the importance of gut microbiota in systemic inflammation and cognitive impairments.
In the realm of TBI, neuroinflammation is a dynamic process involving both peripheral and central immune cells, evolving over time and influencing injury severity and recovery. Hypoxemia post-injury exacerbates neuroinflammation and chronic cognitive deficits, although the exact mechanisms remain unclear. Gut microbiota modulation has emerged as a significant factor in TBI recovery, with changes in gut microbiome composition impacting neuroinflammation, neurogenesis, and long-term outcomes. Interactions between immune cells and gut metabolites, as well as the role of specific T cell subsets, are areas of active investigation.
Moreover, the interorgan connection during critical illness, such as acute kidney injury (AKI), reveals significant insights into CNS inflammation and behaviour changes. Identifying drivers of brain inflammation post-AKI, whether mediated by peripheral immune cells, kidney molecular mediators, or systemic inflammation, is vital for understanding cognitive dysfunction and developing therapeutic strategies.
This Research Topic invites contributions that review current progress and explore innovative angles on immune regulation in AD and TBI. This includes examining roles of microglia, cytokines, and other neuroinflammation axis, and leveraging advanced technologies like single-cell RNA sequencing and imaging to uncover novel regulatory pathways. Manuscripts that elucidate the interplay between systemic and CNS immune responses and propose potential therapeutic targets to modulate immune activity are particularly welcome. By fostering a deeper understanding of these complex neuro-immune interactions, we aim to pave the way for innovative treatments to slow or halt disease progression and improve recovery outcomes.
This Research Topic, seeks Original Research, Review, Mini-Review, Hypothesis and Theory, Perspective, Clinical Trial, Case Report, and Opinion articles that cover, but are not limited to, the following topics:
1. Brain-immune interactions in AD
2. Genetic and epigenetic regulation in microglia in AD
3. Barrier systems
4. Gut-brain interactions
5. Circadian rhythm and Sleep
6. Genetic risk factors and GWAS study
7. New technology in neuroinflammation and studies in AD
Keywords: t-cells, immune, Alzheimer's, traumatic brain injury, AD, TBI, neuro-immune, Hypoxemia post-injury, gut microbiota
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.
