About this Research Topic
Stroke is the second leading cause of death and a major contributor to disability worldwide. Considerable progress has been made in our understanding of the pathophysiology of stroke and treatments.
Stroke causes brain tissue damage, triggers microglial reactivity and immune response. Blood-brain barrier breakdown results in lymphocytes and macrophage infiltration. This inflammatory response contributes to further secondary brain Injury. Inflammation in the brain after stroke involves the initiation, development, and prognosis. Inflammation in the brain is not limited to the penumbra but also spreads to the whole brain and affects the physiological functions of the brain after a stroke. This may lead to dementia, depression, and fatigue after stroke.
Non-neuronal cells such as microglia and astrocytes have crucial functions in CNS and involve in the pathophysiology of stroke. Crosstalk between peripheral immune cells and non-neuronal cells contributes to both repair and damage processes.
Based on the increasing knowledge of mechanisms of ischemic stroke, preserving blood-brain barrier integrity and abrogating the inflammation in stroke may become new effective targets for stroke treatments.
The goal of this research topic is to discuss the role of neuroinflammation in the pathogenic processes and assess the potential therapeutic value, focusing on the BBB and the interactions between the central nervous system and peripheral immune responses. We are looking for Review and Original Research manuscripts focusing on, but not limited to the following topics:
- Non-neuronal cells in stroke - from pathogenesis to biomarkers
- Neuroinflammation, Blood-Brain Barrier dysfunction in Stroke
- Post-stroke depression and Cognitive Impairment: Mechanisms and pharmacological treatment
- Therapy targets of inflammation and immune response and blood-brain barrier damage after stroke, including chemical drugs and natural products
- Molecular Biomarkers in blood, urine, and other body fluids are associated with stroke or cognitive decline after stroke
Stroke causes brain tissue damage, triggers microglial reactivity and immune response. Blood-brain barrier breakdown results in lymphocytes and macrophage infiltration. This inflammatory response contributes to further secondary brain Injury. Inflammation in the brain after stroke involves the initiation, development, and prognosis. Inflammation in the brain is not limited to the penumbra but also spreads to the whole brain and affects the physiological functions of the brain after a stroke. This may lead to dementia, depression, and fatigue after stroke.
Non-neuronal cells such as microglia and astrocytes have crucial functions in CNS and involve in the pathophysiology of stroke. Crosstalk between peripheral immune cells and non-neuronal cells contributes to both repair and damage processes.
Based on the increasing knowledge of mechanisms of ischemic stroke, preserving blood-brain barrier integrity and abrogating the inflammation in stroke may become new effective targets for stroke treatments.
The goal of this research topic is to discuss the role of neuroinflammation in the pathogenic processes and assess the potential therapeutic value, focusing on the BBB and the interactions between the central nervous system and peripheral immune responses. We are looking for Review and Original Research manuscripts focusing on, but not limited to the following topics:
- Non-neuronal cells in stroke - from pathogenesis to biomarkers
- Neuroinflammation, Blood-Brain Barrier dysfunction in Stroke
- Post-stroke depression and Cognitive Impairment: Mechanisms and pharmacological treatment
- Therapy targets of inflammation and immune response and blood-brain barrier damage after stroke, including chemical drugs and natural products
- Molecular Biomarkers in blood, urine, and other body fluids are associated with stroke or cognitive decline after stroke
Keywords: Stroke, Immune, Inflammatory, Blood Brain Barrier, Post-stroke depression and cognitive impairment
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.
