Dementia is a challenging global problem that currently has no cure. The difficulty of treating dementia has been attributed to the unclear etiology and pathogenesis per se. Recent research has shed light on the critical role of inflammation and immunity in cognitive impairment.
Alzheimer’s disease (AD), the most common type of neurodegenerative dementia, is marked as a disease with amyloid and tau pathology. However, it has been noticed that abnormal inflammatory processes occur in the brain and peripheral organs much earlier than these pathological hallmarks. Microglia, the most important resident immune cells of the central nervous system, has been demonstrated to interact with amyloid pathology and regulate AD from disease manifestation to progression. Advances in PET imaging also support the activation of microglial and astroglial cells in early AD. Furthermore, the discovery of the cerebral lymphatic system in 2015 made a breakthrough in the research field of immunity and brain disorders. The dysfunction of clearance of brain hazards is considered a critical factor in AD pathogenesis. Meanwhile, it is well-accepted that T cells interact with amyloid metabolism and contribute to inflammation and neuronal loss in AD.
Vascular dementia (VaD) is another prevalent type of cognitive impairment. Inflammation promotes cerebral vascular dysfunction and thus acts as a critical player in the etiology of VaD. A recent study of post-stroke cognitive impairment (PSCI) revealed that the levels of lipoxin A4, a type of bioactive lipid that promotes the resolution of inflammation, were decreased in the plasma of PSCI patients and correlated to cognitive function.
Overall, inflammation and immunity play key roles in the pathogenesis of dementia, and research in this field will contribute to understanding dementia and treatment innovation. We welcome Review, Mini-Review, Original Research, and Clinical Trial, including basic research to translational studies and clinical investigations about inflammation and immunity in dementia.
Research areas to be covered by this Research Topic include, but are not limited to the following:
- Biomarker studies about inflammation and immunity with regards to the diagnosis of dementia, evaluation of dementia progression
- Original Research and Review about the role of inflammation and immunity in the pathogenesis of dementia, especially about the interaction between peripheral organs, macrophages, and brain microglia, the function of the cerebral lymphatic system, and mechanisms of disturbed resolution of inflammation in dementia
- Treatment studies targeting inflammation and immunity in dementia, e.g., methods based on specialized pro-resolving mediators, novel immunotherapy against Abeta, tau, and immune modulation
- Original Research and Review on the Gut-brain axis and its role in the development of dementia via regulating neuroinflammation and immunity
- Role of the adaptive immune response, e.g., T cell function and pathogen-infection factors in dementia
Dementia is a challenging global problem that currently has no cure. The difficulty of treating dementia has been attributed to the unclear etiology and pathogenesis per se. Recent research has shed light on the critical role of inflammation and immunity in cognitive impairment.
Alzheimer’s disease (AD), the most common type of neurodegenerative dementia, is marked as a disease with amyloid and tau pathology. However, it has been noticed that abnormal inflammatory processes occur in the brain and peripheral organs much earlier than these pathological hallmarks. Microglia, the most important resident immune cells of the central nervous system, has been demonstrated to interact with amyloid pathology and regulate AD from disease manifestation to progression. Advances in PET imaging also support the activation of microglial and astroglial cells in early AD. Furthermore, the discovery of the cerebral lymphatic system in 2015 made a breakthrough in the research field of immunity and brain disorders. The dysfunction of clearance of brain hazards is considered a critical factor in AD pathogenesis. Meanwhile, it is well-accepted that T cells interact with amyloid metabolism and contribute to inflammation and neuronal loss in AD.
Vascular dementia (VaD) is another prevalent type of cognitive impairment. Inflammation promotes cerebral vascular dysfunction and thus acts as a critical player in the etiology of VaD. A recent study of post-stroke cognitive impairment (PSCI) revealed that the levels of lipoxin A4, a type of bioactive lipid that promotes the resolution of inflammation, were decreased in the plasma of PSCI patients and correlated to cognitive function.
Overall, inflammation and immunity play key roles in the pathogenesis of dementia, and research in this field will contribute to understanding dementia and treatment innovation. We welcome Review, Mini-Review, Original Research, and Clinical Trial, including basic research to translational studies and clinical investigations about inflammation and immunity in dementia.
Research areas to be covered by this Research Topic include, but are not limited to the following:
- Biomarker studies about inflammation and immunity with regards to the diagnosis of dementia, evaluation of dementia progression
- Original Research and Review about the role of inflammation and immunity in the pathogenesis of dementia, especially about the interaction between peripheral organs, macrophages, and brain microglia, the function of the cerebral lymphatic system, and mechanisms of disturbed resolution of inflammation in dementia
- Treatment studies targeting inflammation and immunity in dementia, e.g., methods based on specialized pro-resolving mediators, novel immunotherapy against Abeta, tau, and immune modulation
- Original Research and Review on the Gut-brain axis and its role in the development of dementia via regulating neuroinflammation and immunity
- Role of the adaptive immune response, e.g., T cell function and pathogen-infection factors in dementia