The case for blood–brain barrier dysfunction in the pathogenesis of Alzheimer's disease
Identifieur interne : 002A46 ( Main/Corpus ); précédent : 002A45; suivant : 002A47The case for blood–brain barrier dysfunction in the pathogenesis of Alzheimer's disease
Auteurs : Brian Jeynes ; John ProviasSource :
- Journal of Neuroscience Research [ 0360-4012 ] ; 2011-01.
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Abstract
Alzheimer's disease (AD) is a neurodegenerative disease that leads to a progressive loss of integrative and memory capacities of the brain. This is the predominant form of neurodegenerative dementia, with a growing prevalence of between 1 in 50 and 1 in 100 in North America. Numerous hypotheses related to the etiology of AD have developed over the years. However, among the various published hypotheses, the predominant one is related to the progressive and prominent accumulation of central nervous system β‐amyloid peptide and the ensuing brain burden created. It is, therefore, important to consider the homeostatic mechanisms underlying β‐amyloid transport dynamics between the brain and blood vascular compartments. As well, there is a dynamic interrelationship between soluble and insoluble forms of the peptide. Factors that underlie and regulate these dynamic processes are likely relevant to the end accumulation of β‐amyloid peptide in the brain compartment and ultimately in insoluble forms, which is characteristic of, and significant for, the pathophysiology of the Alzheimer's brain. Significantly, and in particular relation to the amyloid burden theory mentioned above, it has been postulated that a dysfunctioning blood–brain barrier (BBB) may play a significant, if not critical, role in the pathogenesis of AD. By allowing the influx of injurious materials or agents into the brain or by impeding or blocking the efflux of those materials and/or agents, BBB‐related neuronopathies and their associated sequelae could, and do, ensue. © 2010 Wiley‐Liss, Inc.
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DOI: 10.1002/jnr.22527
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Res.</title><idno type="ISSN">0360-4012</idno><idno type="eISSN">1097-4547</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2011-01">2011-01</date><biblScope unit="volume">89</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="22">22</biblScope><biblScope unit="page" to="28">28</biblScope></imprint><idno type="ISSN">0360-4012</idno></series><idno type="istex">1F5C00974AA8D0AF9F2548DED03020286EFBD18E</idno><idno type="DOI">10.1002/jnr.22527</idno><idno type="ArticleID">JNR22527</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0360-4012</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Alzheimer's disease</term><term>amyloid</term><term>blood–brain barrier</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Alzheimer's disease (AD) is a neurodegenerative disease that leads to a progressive loss of integrative and memory capacities of the brain. 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Significantly, and in particular relation to the amyloid burden theory mentioned above, it has been postulated that a dysfunctioning blood–brain barrier (BBB) may play a significant, if not critical, role in the pathogenesis of AD. By allowing the influx of injurious materials or agents into the brain or by impeding or blocking the efflux of those materials and/or agents, BBB‐related neuronopathies and their associated sequelae could, and do, ensue. © 2010 Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Brian Jeynes</name><affiliations><json:string>Faculty of Applied Health Sciences, Brock University, St. Catharine's, Ontario, Canada</json:string></affiliations></json:item><json:item><name>John Provias</name><affiliations><json:string>Department of Pathology and Molecular Medicine (Neuropathology), Hamilton Health Sciences, McMaster University, Hamilton, Ontario, Canada</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>blood–brain barrier</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>amyloid</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Alzheimer's disease</value></json:item></subject><articleId><json:string>JNR22527</json:string></articleId><language><json:string>eng</json:string></language><abstract>Alzheimer's disease (AD) is a neurodegenerative disease that leads to a progressive loss of integrative and memory capacities of the brain. 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Significantly, and in particular relation to the amyloid burden theory mentioned above, it has been postulated that a dysfunctioning blood–brain barrier (BBB) may play a significant, if not critical, role in the pathogenesis of AD. 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This is the predominant form of neurodegenerative dementia, with a growing prevalence of between 1 in 50 and 1 in 100 in North America. Numerous hypotheses related to the etiology of AD have developed over the years. However, among the various published hypotheses, the predominant one is related to the progressive and prominent accumulation of central nervous system β‐amyloid peptide and the ensuing brain burden created. It is, therefore, important to consider the homeostatic mechanisms underlying β‐amyloid transport dynamics between the brain and blood vascular compartments. As well, there is a dynamic interrelationship between soluble and insoluble forms of the peptide. Factors that underlie and regulate these dynamic processes are likely relevant to the end accumulation of β‐amyloid peptide in the brain compartment and ultimately in insoluble forms, which is characteristic of, and significant for, the pathophysiology of the Alzheimer's brain. Significantly, and in particular relation to the amyloid burden theory mentioned above, it has been postulated that a dysfunctioning blood–brain barrier (BBB) may play a significant, if not critical, role in the pathogenesis of AD. By allowing the influx of injurious materials or agents into the brain or by impeding or blocking the efflux of those materials and/or agents, BBB‐related neuronopathies and their associated sequelae could, and do, ensue. © 2010 Wiley‐Liss, Inc.</abstract><subject lang="en"><genre>Keywords</genre><topic>blood–brain barrier</topic><topic>amyloid</topic><topic>Alzheimer's disease</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Neuroscience Research</title></titleInfo><titleInfo type="abbreviated"><title>J. Neurosci. 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