About this Research Topic
Neurovascular unit (NVU) is a concept introduced in 2001 that emphasizes the close link between neurons and their vessels. Since then, the NVU caught neuroscientists’ attention resulting in considerable advances in this field.
The NVU is a functional unit composed of neurons and non-neuronal cells, such as vascular cells (endothelia, pericytes, and vascular smooth muscle cells) and glia (astrocytes, microglia, and oligodendroglia). The interaction between all these cell types contributes to the maintenance of central nervous system homeostasis, while abnormal regulation may lead to cerebral dysfunction and diseases. Previously, NVU dysfunction was mainly studied in cerebrovascular diseases, especially ischemic stroke. Recently, the role of NVU in neurodegeneration progressively moved in the spotlight leading to the creation of a new research area on Alzheimer's etiology.
The vascular hypothesis states that a primary impairment at the neurovascular coupling level occurs and may induce various dysfunctions like an insufficient cerebral perfusion pressure, a dysregulation of neurogenic regions and/or neural activity. This neurovascular alteration might subsequently release toxic components, breakdown the blood-brain barrier and/or induce neuronal losses. Recent and various studies have been dedicated to better understanding the potentially deleterious impact of a defective NVU in neurodegenerative diseases. Despite these efforts, biological mechanisms behind these dynamic changes as well as the real impact of an abnormal NVU on the disease’s progression remain unclear both in vivo and in vitro.
This Research Topic aims to provide an overview of the NVU’s role in the development and progression of neurodegenerative diseases, such as Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis, and stroke. Articles focusing on biomarkers, genetical aspects and/or neuroimaging reflecting the dynamic changes of NVU damage in vivo and in vitro are also welcome. Although this Research Topic mainly focuses on the NVU changes, we also welcome studies related to NVU and interaction with inflammation and innate immunity cells.
The NVU is a functional unit composed of neurons and non-neuronal cells, such as vascular cells (endothelia, pericytes, and vascular smooth muscle cells) and glia (astrocytes, microglia, and oligodendroglia). The interaction between all these cell types contributes to the maintenance of central nervous system homeostasis, while abnormal regulation may lead to cerebral dysfunction and diseases. Previously, NVU dysfunction was mainly studied in cerebrovascular diseases, especially ischemic stroke. Recently, the role of NVU in neurodegeneration progressively moved in the spotlight leading to the creation of a new research area on Alzheimer's etiology.
The vascular hypothesis states that a primary impairment at the neurovascular coupling level occurs and may induce various dysfunctions like an insufficient cerebral perfusion pressure, a dysregulation of neurogenic regions and/or neural activity. This neurovascular alteration might subsequently release toxic components, breakdown the blood-brain barrier and/or induce neuronal losses. Recent and various studies have been dedicated to better understanding the potentially deleterious impact of a defective NVU in neurodegenerative diseases. Despite these efforts, biological mechanisms behind these dynamic changes as well as the real impact of an abnormal NVU on the disease’s progression remain unclear both in vivo and in vitro.
This Research Topic aims to provide an overview of the NVU’s role in the development and progression of neurodegenerative diseases, such as Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis, and stroke. Articles focusing on biomarkers, genetical aspects and/or neuroimaging reflecting the dynamic changes of NVU damage in vivo and in vitro are also welcome. Although this Research Topic mainly focuses on the NVU changes, we also welcome studies related to NVU and interaction with inflammation and innate immunity cells.
Keywords: Neurovascular Unit, Neurodegeneration, Ischemia, Inflammation, Genetic
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