Neuroinflammation plays a fundamental role in mediating the onset and progression of aging, especially cellular senescence of the central nervous system. It is also a hallmark of neurodegenerative diseases and chronic brain injury, which is led by traumatic brain injury (chronic traumatic encephalopathy), brain vascular diseases, carotid artery stenosis-induced brain ischemia, and stroke (ischemic/hemorrhagic). In all these conditions, the cellular and molecular mechanisms underlying the occurrence and development of neuroinflammation are still expected to be fully elucidated. These mechanisms may include inflammatory cell death, production, and secretion of senescent-associated secretory phenotype (SASP), neutrophil extracellular traps (NETs), mitochondrial damage, Endoplasmic reticulum stress, blood-brain barrier damage, immune regulation, deposition and clearance of pathological proteins, etc.
Furthermore, brain aging contributes to immune system aging, including aging-related changes in the immune system. In turn, systemic aging, which is the source of chronic inflammation in the elderly, results in brain aging and memory loss in a reciprocal manner. Consequently, immunotherapeutics such as inflammation modulation, cellular immune regulation, and protective autoimmunity may provide promising approaches to rejuvenate neuroinflammatory disorders and repair chronic brain injury. However, the mutual impact between aging and chronic brain injury still lacks study, which limits the exploitation of novel therapeutic avenues for elderly people in the future.
With the development of neuroimaging, next-generation sequencing technologies, bioinformatics, and interdisciplinary joint research has become the mainstream developing trend in neuroscience. For example, single-cell sequencing, transcriptome sequencing, proteome sequencing, and metabolomic profiling provide powerful tools to allow the overall investigation of the cellular and molecular mechanism underlying the development of aging and brain diseases. Neuroscientists need to cooperate with bioinformatics scientists to complete the multi-omics analysis, in order to obtain more opportunities to develop novel therapeutic strategies for cognitive dysfunction. Consequently, researchers should actively break the disciplinary barriers and strengthen communication between clinical and basic medical research.
This research topic will focus on the frontier studies on the pathological mechanism underlying aging and chronic brain injury, as well as their interactions. We hope the submissions can expand our previous understanding of the diseases, thus exploring promising therapeutic strategies for clinical application.
We welcome research of basic study and clinical study, and consider all submissions in the form of Original Research and Review.
This research topic focuses on, but is not limited to:
Roles and mechanisms of neuroinflammation in the development of chronic brain injury, including traumatic brain injury (chronic traumatic encephalopathy), brain vascular diseases, carotid artery stenosis, and stroke (ischemic/hemorrhagic).
Roles and mechanisms of neuroinflammation in the development of aging and neurodegenerative diseases.
Roles and mechanisms of neuroinflammation underlying the mutual impact between aging and chronic brain injury
Identify the common and disease-specific features of neuroinflammation among various pathological conditions of chronic brain injury.
Clinical biomarkers for diagnosis or outcome prediction associated with neuroinflammation for chronic brain injury, aging, and neurodegenerative diseases.
Translational research or in-vivo research of novel immuno-inflammatory therapy for chronic brain injury, cellular senescence, and neurodegeneration.
Neuroinflammation plays a fundamental role in mediating the onset and progression of aging, especially cellular senescence of the central nervous system. It is also a hallmark of neurodegenerative diseases and chronic brain injury, which is led by traumatic brain injury (chronic traumatic encephalopathy), brain vascular diseases, carotid artery stenosis-induced brain ischemia, and stroke (ischemic/hemorrhagic). In all these conditions, the cellular and molecular mechanisms underlying the occurrence and development of neuroinflammation are still expected to be fully elucidated. These mechanisms may include inflammatory cell death, production, and secretion of senescent-associated secretory phenotype (SASP), neutrophil extracellular traps (NETs), mitochondrial damage, Endoplasmic reticulum stress, blood-brain barrier damage, immune regulation, deposition and clearance of pathological proteins, etc.
Furthermore, brain aging contributes to immune system aging, including aging-related changes in the immune system. In turn, systemic aging, which is the source of chronic inflammation in the elderly, results in brain aging and memory loss in a reciprocal manner. Consequently, immunotherapeutics such as inflammation modulation, cellular immune regulation, and protective autoimmunity may provide promising approaches to rejuvenate neuroinflammatory disorders and repair chronic brain injury. However, the mutual impact between aging and chronic brain injury still lacks study, which limits the exploitation of novel therapeutic avenues for elderly people in the future.
With the development of neuroimaging, next-generation sequencing technologies, bioinformatics, and interdisciplinary joint research has become the mainstream developing trend in neuroscience. For example, single-cell sequencing, transcriptome sequencing, proteome sequencing, and metabolomic profiling provide powerful tools to allow the overall investigation of the cellular and molecular mechanism underlying the development of aging and brain diseases. Neuroscientists need to cooperate with bioinformatics scientists to complete the multi-omics analysis, in order to obtain more opportunities to develop novel therapeutic strategies for cognitive dysfunction. Consequently, researchers should actively break the disciplinary barriers and strengthen communication between clinical and basic medical research.
This research topic will focus on the frontier studies on the pathological mechanism underlying aging and chronic brain injury, as well as their interactions. We hope the submissions can expand our previous understanding of the diseases, thus exploring promising therapeutic strategies for clinical application.
We welcome research of basic study and clinical study, and consider all submissions in the form of Original Research and Review.
This research topic focuses on, but is not limited to:
Roles and mechanisms of neuroinflammation in the development of chronic brain injury, including traumatic brain injury (chronic traumatic encephalopathy), brain vascular diseases, carotid artery stenosis, and stroke (ischemic/hemorrhagic).
Roles and mechanisms of neuroinflammation in the development of aging and neurodegenerative diseases.
Roles and mechanisms of neuroinflammation underlying the mutual impact between aging and chronic brain injury
Identify the common and disease-specific features of neuroinflammation among various pathological conditions of chronic brain injury.
Clinical biomarkers for diagnosis or outcome prediction associated with neuroinflammation for chronic brain injury, aging, and neurodegenerative diseases.
Translational research or in-vivo research of novel immuno-inflammatory therapy for chronic brain injury, cellular senescence, and neurodegeneration.
