Dysregulation of neuroimmune signaling plays an important role in promoting vascular cognitive impairment and dementia (VCID). Active research at the frontiers of neuroscience and immunology has highlighted the alterations in brain-resident microglia, astrocytes, and peripheral immune cells (neutrophils, monocytes, T cells, and B cells), as well as crosstalk between innate and adaptive immune cells in the development of neuropathology in different entities such as mild cognitive impairment (MCI), Alzheimer's disease (AD), vascular cognitive disorders (VaD), etc. Together with M1-type (pro-inflammatory) and M2-type (neuroprotective) microglia, single-cell transcriptomic studies have identified many functionally distinct microglial subsets in healthy and dementia brains, including disease-associated microglia (DAM), microglia neurodegenerative phenotype (MGnD), and morphologically activated microglia (PAM). Emerging evidence revealed key gene characteristics and communication points between novel microglial cell populations. For example, genes upregulated in DAM include several known AD risk genes, such as APOE and TREM2. Major players in transforming homeostatic microglia into MGnD are managed by the APOE/TREM2/CD33 pathway. Astrocytes with high heterogeneity are closely connected with microglial activation, pro-inflammatory monocyte recruitment, neurotoxic and inflammatory factor production, and boosting brain pathology by various immune-inflammatory mechanisms. Thus, deep and continued research in this area promises to establish immune-based therapies for re-establishing brain function in VCID.
This Research Topic aims to provide a forum to advance research on the contribution of neuroimmune signaling, disease-specific microglia phenotypes, and molecular genetic markers and their crosstalks between the peripheral immune system and the brain to the genesis and development of VCID and focuses on the latest progress in the potential of innovative immune-based pharmacological interventions and the development of drugs targeting neuroimmune inflammation, which will help achieve a beneficial impact on the pathogenesis and therapeutic discovery of VCID. The submission of original research, review, systematic review, mini review, perspective, opinion, and data report covering, but not limited to, the following subtopics are all welcome:
1) Novel findings on neuroimmune alterations in the function of microglia, astrocytes, and other brain cells, as well as the intersection between the peripheral immune system and the brain and how they affect cognition;
2) Impact of aging and how endocrine aging (e.g., menopause) affects cognitive status by influencing the immune response;
3) Key findings of promising blood and brain biomarkers, innovative brain imaging, and multi-omics studies underlying neuroimmune inflammation for predicting the early onset of VCID;
4) Discovery of immune-based drug molecules and therapies to improve brain function for the treatment of different entities in VCID;
5) Advances in ongoing clinical trials and their promise for improving brain function underlying neuroimmune inflammation.
Dysregulation of neuroimmune signaling plays an important role in promoting vascular cognitive impairment and dementia (VCID). Active research at the frontiers of neuroscience and immunology has highlighted the alterations in brain-resident microglia, astrocytes, and peripheral immune cells (neutrophils, monocytes, T cells, and B cells), as well as crosstalk between innate and adaptive immune cells in the development of neuropathology in different entities such as mild cognitive impairment (MCI), Alzheimer's disease (AD), vascular cognitive disorders (VaD), etc. Together with M1-type (pro-inflammatory) and M2-type (neuroprotective) microglia, single-cell transcriptomic studies have identified many functionally distinct microglial subsets in healthy and dementia brains, including disease-associated microglia (DAM), microglia neurodegenerative phenotype (MGnD), and morphologically activated microglia (PAM). Emerging evidence revealed key gene characteristics and communication points between novel microglial cell populations. For example, genes upregulated in DAM include several known AD risk genes, such as APOE and TREM2. Major players in transforming homeostatic microglia into MGnD are managed by the APOE/TREM2/CD33 pathway. Astrocytes with high heterogeneity are closely connected with microglial activation, pro-inflammatory monocyte recruitment, neurotoxic and inflammatory factor production, and boosting brain pathology by various immune-inflammatory mechanisms. Thus, deep and continued research in this area promises to establish immune-based therapies for re-establishing brain function in VCID.
This Research Topic aims to provide a forum to advance research on the contribution of neuroimmune signaling, disease-specific microglia phenotypes, and molecular genetic markers and their crosstalks between the peripheral immune system and the brain to the genesis and development of VCID and focuses on the latest progress in the potential of innovative immune-based pharmacological interventions and the development of drugs targeting neuroimmune inflammation, which will help achieve a beneficial impact on the pathogenesis and therapeutic discovery of VCID. The submission of original research, review, systematic review, mini review, perspective, opinion, and data report covering, but not limited to, the following subtopics are all welcome:
1) Novel findings on neuroimmune alterations in the function of microglia, astrocytes, and other brain cells, as well as the intersection between the peripheral immune system and the brain and how they affect cognition;
2) Impact of aging and how endocrine aging (e.g., menopause) affects cognitive status by influencing the immune response;
3) Key findings of promising blood and brain biomarkers, innovative brain imaging, and multi-omics studies underlying neuroimmune inflammation for predicting the early onset of VCID;
4) Discovery of immune-based drug molecules and therapies to improve brain function for the treatment of different entities in VCID;
5) Advances in ongoing clinical trials and their promise for improving brain function underlying neuroimmune inflammation.