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Neurovascular disease: 2022 update
1Department of Neurology, McGovern Medical School, UTHealth Houston and Memorial Hermann Hospital, Houston, Texas, USA.
Insights
Recent research explores vascular disease, focusing on brain malformations and the brain-immune system crosstalk after injury. Key findings include T cell involvement in white matter repair and novel insights into B cell roles in neuroinflammation and vascular dementia.
Area of Science:
- Neuroscience
- Immunology
- Vascular Biology
Background:
- Vascular malformations like brain arteriovenous malformations and cerebral cavernous malformations can cause severe brain injury.
- The interplay between the brain and immune system following brain injury, such as stroke, is a critical area of research.
- Understanding the cellular and molecular mechanisms underlying vascular diseases is essential for developing effective treatments.
Purpose of the Study:
- To review recent advancements in vascular disease research, highlighting key findings in pathogenesis, immune response, and cellular contributions.
- To explore the role of immune cells, including T cells, B cells, and myeloid cells, in brain injury and repair.
- To investigate the contribution of senescent cells and pericytes to vascular aging and brain function.
Main Methods:
- Review and synthesis of recent publications on vascular disease, brain injury, and neuroinflammation.
- Analysis of studies investigating the cellular mechanisms of vascular malformations and their neurological complications.
- Examination of research on immune cell infiltration and function within the central nervous system (CNS) after injury.
- Evaluation of studies on cellular senescence and pericyte function in the context of vascular health.
Main Results:
- T cells, in conjunction with microglia, play a role in white matter repair after ischemic injury, demonstrating innate-adaptive immune crosstalk.
- Antigen-experienced B cells from meninges and skull bone marrow, not blood-derived B cells, are implicated in neuroinflammation, suggesting novel roles in vascular dementia.
- CNS-infiltrating myeloid cells can originate from brain border tissues and possess distinct transcriptional profiles.
- Microglia contribute to amyloid deposition, and perivascular amyloid-beta clearance mechanisms are explored in cerebral amyloid angiopathy.
- Senescent endothelial cells, modeled using Hutchinson-Gilford progeria syndrome, suggest therapeutic potential in targeting telomere shortening.
- Capillary pericytes are shown to regulate basal cerebral blood flow resistance and modulation.
Conclusions:
- Recent research has significantly advanced our understanding of vascular disease pathogenesis and the complex brain-immune interactions post-injury.
- Novel insights into the roles of T cells, B cells, and myeloid cells offer new avenues for therapeutic intervention in stroke and neurodegenerative diseases.
- The study of cellular senescence and pericytes provides potential strategies for combating vascular aging and maintaining brain health.
- Several identified therapeutic strategies hold promise for translation into clinical applications for vascular disease management.
Abstract:
In this update we present a series of papers focused on topics that have emerged in vascular disease over the prior year. The first two papers focus on the pathogenesis of vascular malformations, the first on brain arteriovenous malformations, and the second on cerebral cavernous malformations. These disorders can lead to significant brain injuries from intracerebral hemorrhage (if they rupture) or other neurological complications, including seizures. The next set of papers reflects work that has advanced our understanding of how the brain and the immune system "communicate" after brain injury, including stroke (papers 3-6). The first of these shows that T cells are involved in white matter repair after ischemic injury, an effect dependent on microglia, demonstrating the important cross-talk between innate and adaptive immunity. The next two papers focus on B cells, which have been relatively understudied in the context of brain injury. The contribution of antigen-experienced B cells from the meninges and skull bone marrow, rather than blood-derived B cells in neuroinflammation opens up a very novel area of investigation. The possibility that antibody secreting B cells may contribute to vascular dementia will certainly be an active area for future investigations. Similarly, in paper 6, investigators found that CNS-infiltrating myeloid cells can originate from brain borders tissues. These cells have unique transcriptional signatures that are distinct from their blood-derived counterparts, and likely contribute to myeloid cell infiltration from bone-marrow niches in close proximity to the brain. The contribution of microglia, the primary innate immune cell of the brain, to amyloid deposition and propagation is then discussed, followed by work on how perivascular Aβ is potentially cleared along the cerebral vessels in patients with cerebral amyloid angiopathy. The final two papers focus on the contribution of senescent endothelial cells and pericytes. The first used a model of accelerated senescence (Hutchinson-Gilford progeria syndrome; HGPS) and shows the translational potential of an approach to reduce telomere shortening to slow aging. The final paper demonstrates how capillary pericytes contribute to basal blood flow resistance and slow modulation of blood flow throughout the brain. Interestingly, several of the papers identified therapeutic strategies that could be potentially translated into clinical populations.
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