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http://purl.uniprot.org/citations/24739782http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24739782http://www.w3.org/2000/01/rdf-schema#comment"

Objective

A significant cause of spontaneous hemorrhages in the elderly is cerebral amyloid angiopathy (CAA), which causes degeneration of cerebral vessels, but the mechanisms are unclear.

Methods

We isolated leptomeningeal vessels from rapidly autopsied brains (the average of postmortem intervals was 3.28 hours) from 9 patients with CAA and 10 age-matched controls, and used molecular, cell biology, and immunohistochemical approaches to examine β-site APP-cleaving enzyme 1 (BACE1) protein expression and enzymatic activities as well as tight junction molecular components in small- and medium-sized arteries of the cerebral cortex and leptomeninges.

Results

We not only identified that the cerebral vessels, including leptomeningeal and cortical vessels, synthesize and express BACE1, but also found a significant elevation of both BACE1 protein levels and enzymatic activities in leptomeningeal vessels from patients with CAA. Moreover, overexpression of BACE1 in endothelial cells resulted in a significant reduction of occludin, a tight junction protein in blood vessels.

Conclusion

These findings suggest that in addition to neurons, cerebral vascular cells express functional BACE1. Moreover, elevated vascular BACE1 may contribute to deficiency of occludin in cerebral vessels, which ultimately has a critical role in pathogenesis of CAA and its related hemorrhage."xsd:string
http://purl.uniprot.org/citations/24739782http://purl.org/dc/terms/identifier"doi:10.1212/wnl.0000000000000403"xsd:string
http://purl.uniprot.org/citations/24739782http://purl.uniprot.org/core/author"Cheng X."xsd:string
http://purl.uniprot.org/citations/24739782http://purl.uniprot.org/core/author"Li R."xsd:string
http://purl.uniprot.org/citations/24739782http://purl.uniprot.org/core/author"Shen Y."xsd:string
http://purl.uniprot.org/citations/24739782http://purl.uniprot.org/core/author"Yao H."xsd:string
http://purl.uniprot.org/citations/24739782http://purl.uniprot.org/core/author"He P."xsd:string
http://purl.uniprot.org/citations/24739782http://purl.uniprot.org/core/author"Dong Q."xsd:string
http://purl.uniprot.org/citations/24739782http://purl.uniprot.org/core/date"2014"xsd:gYear
http://purl.uniprot.org/citations/24739782http://purl.uniprot.org/core/name"Neurology"xsd:string
http://purl.uniprot.org/citations/24739782http://purl.uniprot.org/core/pages"1707-1715"xsd:string
http://purl.uniprot.org/citations/24739782http://purl.uniprot.org/core/title"Occludin deficiency with BACE1 elevation in cerebral amyloid angiopathy."xsd:string
http://purl.uniprot.org/citations/24739782http://purl.uniprot.org/core/volume"82"xsd:string
http://purl.uniprot.org/citations/24739782http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/24739782
http://purl.uniprot.org/citations/24739782http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/24739782
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http://purl.uniprot.org/uniprot/#_Q16625-mappedCitation-24739782http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24739782
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http://purl.uniprot.org/uniprot/#_Q8IYC8-mappedCitation-24739782http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24739782
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