In recent years, immunological research in the nervous system has gone beyond the study of defense against virus infections or autoimmune diseases such as multiple sclerosis.
Neuroinflammation has been indeed identified in the pathogenesis of many diseases that were previously considered unrelated to immune mechanisms, such as Alzheimer's disease, Parkinson's disease, and epilepsy. Recent findings indicate that immune cells not only disrupt the nervous system but also interfere with the proliferation of neural stem cells in the context of these diseases.
It has been observed that patients affected by neuroinflammatory diseases generally have vascular lesions in the brain. Cerebrovascular dysfunction may, therefore, precede immune response and nervous system damage.
Inflammation, trauma and neurodegenerative diseases often occur because of increased permeability of the blood-brain barrier (BBB), which is a cell complex composed of non-fenestrated endothelial cells, pericytes, a basement membrane, and astrocytic endfeet. For example, post-stroke immune activation may be due to the destruction of the BBB, which allows immune-isolated central nervous system antigens to contact the systemic immune system.
The structural integrity of the BBB is therefore of crucial importance. When this is changed, peripheral T lymphocytic cells migrate into the brain parenchyma, which results in the release of pro-inflammatory factors, and consequent loss of tight junction molecules including occludins and adhesion proteins. This causes, in turn, a reduction in the synthesis of type IV collagen and laminin and therefore further degradation of the BBB integrity.
In Alzheimer’s disease, BBB lesions have been found to accelerate the aggregation and deposition of the amyloid-beta (Aß) protein, reduce its clearance, and promote the pathogenesis of the disease. However, there are still many important questions to be answered, due to the complexity of neurovascular interactions.
This Research Topic aims to study the neurovascular changes involved in neuroinflammatory diseases, which may lead us to identify new therapeutic targets that play a role in regulating the progression or delaying the onset of these diseases as well as in repairing or protecting the central nervous system.
Potential topics include but are not limited to the following:
• Neurovascular changes in different neuroinflammation phases;
• Heterogeneity of immune cells that are involved in neurodegenerative diseases;
• The role of glial cells in the BBB, in the context of neurodegenerative diseases;
• Novel experimental models used to study the role of inflammation in neurodegenerative diseases;
• Therapeutic strategies that might modulate the integrity of BBB.
In recent years, immunological research in the nervous system has gone beyond the study of defense against virus infections or autoimmune diseases such as multiple sclerosis.
Neuroinflammation has been indeed identified in the pathogenesis of many diseases that were previously considered unrelated to immune mechanisms, such as Alzheimer's disease, Parkinson's disease, and epilepsy. Recent findings indicate that immune cells not only disrupt the nervous system but also interfere with the proliferation of neural stem cells in the context of these diseases.
It has been observed that patients affected by neuroinflammatory diseases generally have vascular lesions in the brain. Cerebrovascular dysfunction may, therefore, precede immune response and nervous system damage.
Inflammation, trauma and neurodegenerative diseases often occur because of increased permeability of the blood-brain barrier (BBB), which is a cell complex composed of non-fenestrated endothelial cells, pericytes, a basement membrane, and astrocytic endfeet. For example, post-stroke immune activation may be due to the destruction of the BBB, which allows immune-isolated central nervous system antigens to contact the systemic immune system.
The structural integrity of the BBB is therefore of crucial importance. When this is changed, peripheral T lymphocytic cells migrate into the brain parenchyma, which results in the release of pro-inflammatory factors, and consequent loss of tight junction molecules including occludins and adhesion proteins. This causes, in turn, a reduction in the synthesis of type IV collagen and laminin and therefore further degradation of the BBB integrity.
In Alzheimer’s disease, BBB lesions have been found to accelerate the aggregation and deposition of the amyloid-beta (Aß) protein, reduce its clearance, and promote the pathogenesis of the disease. However, there are still many important questions to be answered, due to the complexity of neurovascular interactions.
This Research Topic aims to study the neurovascular changes involved in neuroinflammatory diseases, which may lead us to identify new therapeutic targets that play a role in regulating the progression or delaying the onset of these diseases as well as in repairing or protecting the central nervous system.
Potential topics include but are not limited to the following:
• Neurovascular changes in different neuroinflammation phases;
• Heterogeneity of immune cells that are involved in neurodegenerative diseases;
• The role of glial cells in the BBB, in the context of neurodegenerative diseases;
• Novel experimental models used to study the role of inflammation in neurodegenerative diseases;
• Therapeutic strategies that might modulate the integrity of BBB.