Blood-brain barrier integrity in the pathogenesis of Alzheimer's disease.

Huang, Z; Wong, L-W; Su, Y; Huang, X; Wang, N; Chen, H; Yi, C

Blood-brain barrier integrity in the pathogenesis of Alzheimer's disease.

Huang, Z Wong, L-W Su, Y Huang, X Wang, N Chen, H

Yi, C

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Publisher:: Elsevier BV
Publication Type:: Journal Article
Citation:: Frontiers in neuroendocrinology, 2020, 59
Issue Date:: 2020-08-08

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Field	Value	Language
dc.contributor.author	Huang, Z
dc.contributor.author	Wong, L-W
dc.contributor.author	Su, Y
dc.contributor.author	Huang, X
dc.contributor.author	Wang, N
dc.contributor.author	Chen, H https://orcid.org/0000-0001-6883-3752
dc.contributor.author	Yi, C
dc.date.accessioned	2020-11-05T04:47:46Z
dc.date.available	2020-07-29
dc.date.available	2020-11-05T04:47:46Z
dc.date.issued	2020-08-08
dc.identifier.citation	Frontiers in neuroendocrinology, 2020, 59
dc.identifier.issn	0091-3022
dc.identifier.issn	1095-6808
dc.identifier.uri	http://hdl.handle.net/10453/143765
dc.description.abstract	The blood-brain barrier (BBB) tightly controls the molecular exchange between the brain parenchyma and blood. Accumulated evidence from transgenic animal Alzheimer's disease (AD) models and human AD patients have demonstrated that BBB dysfunction is a major player in AD pathology. In this review, we discuss the role of the BBB in maintaining brain integrity and how this is mediated by crosstalk between BBB-associated cells within the neurovascular unit (NVU). We then discuss the role of the NVU, in particular its endothelial cell, pericyte, and glial cell constituents, in AD pathogenesis. The effect of substances released by the neuroendocrine system in modulating BBB function and AD pathogenesis is also discussed. We perform a systematic review of currently available AD treatments specifically targeting pericytes and BBB glial cells. In summary, this review provides a comprehensive overview of BBB dysfunction in AD and a new perspective on the development of therapeutics for AD.
dc.format	Print-Electronic
dc.language	eng
dc.publisher	Elsevier BV
dc.relation.ispartof	Frontiers in neuroendocrinology
dc.relation.isbasedon	10.1016/j.yfrne.2020.100857
dc.rights	info:eu-repo/semantics/embargoedAccess
dc.subject	1103 Clinical Sciences, 1109 Neurosciences
dc.subject.classification	Endocrinology & Metabolism
dc.title	Blood-brain barrier integrity in the pathogenesis of Alzheimer's disease.
dc.type	Journal Article
utslib.citation.volume	59
utslib.location.activity	United States
utslib.for	1103 Clinical Sciences
utslib.for	1109 Neurosciences
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Strength - CHT - Health Technologies
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
pubs.organisational-group	/University of Technology Sydney
utslib.copyright.status	open_access	*
pubs.consider-herdc	false
utslib.copyright.embargo	2022-08-01T00:00:00+1000Z
dc.date.updated	2020-11-05T04:47:43Z
pubs.publication-status	Published
pubs.volume	59

Abstract:

The blood-brain barrier (BBB) tightly controls the molecular exchange between the brain parenchyma and blood. Accumulated evidence from transgenic animal Alzheimer's disease (AD) models and human AD patients have demonstrated that BBB dysfunction is a major player in AD pathology. In this review, we discuss the role of the BBB in maintaining brain integrity and how this is mediated by crosstalk between BBB-associated cells within the neurovascular unit (NVU). We then discuss the role of the NVU, in particular its endothelial cell, pericyte, and glial cell constituents, in AD pathogenesis. The effect of substances released by the neuroendocrine system in modulating BBB function and AD pathogenesis is also discussed. We perform a systematic review of currently available AD treatments specifically targeting pericytes and BBB glial cells. In summary, this review provides a comprehensive overview of BBB dysfunction in AD and a new perspective on the development of therapeutics for AD.

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http://hdl.handle.net/10453/143765