Pathophysiology of the neurovascular unit: disease cause or consequence?

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Journal titleJournal of Cerebral Blood Flow & Metabolism
Pages12071221; # of pages: 15
SubjectAlzheimer's disease; blood–brain barrier; genetic vasculopathies; migraine; neurovascular unit; seizures
AbstractPathophysiology of the neurovascular unit (NVU) is commonly seen in neurological diseases. The typical features of NVU pathophysiology include tissue hypoxia, inflammatory and angiogenic activation, as well as initiation of complex molecular interactions between cellular (brain endothelial cells, astroctyes, pericytes, inflammatory cells, and neurons) and acellular (basal lamina) components of the NVU, jointly resulting in increased blood–brain barrier permeability, brain edema, neurovascular uncoupling, and neuronal dysfunction and damage. The evidence of important role of the brain vascular compartment in disease pathogenesis has elicited the debate whether the primary vascular events may be a cause of the neurological disease, as opposed to a mere participant recruited by a primary neuronal origin of pathology? Whereas some hereditary and acquired cerebral angiopathies could be considered a primary cause of neurological symptoms of the disease, the epidemiological studies showing a high degree of comorbidity among vascular disease and dementias, including Alzheimer's disease, as well as migraine and epilepsy, suggested that primary vascular pathology may be etiological factor causing neuronal dysfunction or degeneration in these diseases. This review focuses on recent hypotheses and evidence, suggesting that pathophysiology of the NVU may be initiating trigger for neuronal pathology and subsequent neurological manifestations of the disease.
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AffiliationNRC Institute for Biological Sciences; National Research Council Canada
Peer reviewedYes
NPARC number21268914
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Record identifier45393d67-ec64-4373-82a4-371cbc77b25f
Record created2013-11-25
Record modified2016-05-09
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