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Blood-brain barrier...
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van Assema, Danielle M. E.
(author)
Blood-brain barrier P-glycoprotein function in Alzheimer's disease
- Article/chapterEnglish2012
Publisher, publication year, extent ...
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2011-11-25
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Oxford University Press (OUP),2012
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printrdacarrier
Numbers
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LIBRIS-ID:oai:DiVA.org:uu-169981
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https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-169981URI
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https://doi.org/10.1093/brain/awr298DOI
Supplementary language notes
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Language:English
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Summary in:English
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Classification
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
Notes
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A major pathological hallmark of Alzheimer's disease is accumulation of amyloid-beta in senile plaques in the brain. Evidence is accumulating that decreased clearance of amyloid-beta from the brain may lead to these elevated amyloid-beta levels. One of the clearance pathways of amyloid-beta is transport across the blood-brain barrier via efflux transporters. P-glycoprotein, an efflux pump highly expressed at the endothelial cells of the blood-brain barrier, has been shown to transport amyloid-beta. P-glycoprotein function can be assessed in vivo using (R)-[C-11]verapamil and positron emission tomography. The aim of this study was to assess blood-brain barrier P-glycoprotein function in patients with Alzheimer's disease compared with age-matched healthy controls using (R)-[C-11]verapamil and positron emission tomography. In 13 patients with Alzheimer's disease (age 65 +/- 7 years, Mini-Mental State Examination 23 +/- 3), global (R)-[C-11]verapamil binding potential values were increased significantly (P = 0.001) compared with 14 healthy controls (aged 62 +/- 4 years, Mini-Mental State Examination 30 +/- 1). Global (R)-[C-11]verapamil binding potential values were 2.18 +/- 0.25 for patients with Alzheimer's disease and 1.77 +/- 0.41 for healthy controls. In patients with Alzheimer's disease, higher (R)-[C-11]verapamil binding potential values were found for frontal, parietal, temporal and occipital cortices, and posterior and anterior cingulate. No significant differences between groups were found for medial temporal lobe and cerebellum. These data show altered kinetics of (R)-[C-11]verapamil in Alzheimer's disease, similar to alterations seen in studies where P-glycoprotein is blocked by a pharmacological agent. As such, these data indicate that P-glycoprotein function is decreased in patients with Alzheimer's disease. This is the first direct evidence that the P-glycoprotein transporter at the blood-brain barrier is compromised in sporadic Alzheimer's disease and suggests that decreased P-glycoprotein function may be involved in the pathogenesis of Alzheimer's disease.
Subject headings and genre
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P-glycoprotein
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blood-brain barrier
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PET
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Alzheimer's disease
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(R)-[C-11]verapamil
Added entries (persons, corporate bodies, meetings, titles ...)
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Lubberink, MarkUppsala universitet,Enheten för nuklearmedicin och PET(Swepub:uu)marklubb
(author)
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Bauer, Martin
(author)
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van der Flier, Wiesje M.
(author)
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Schuit, Robert C.
(author)
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Windhorst, Albert D.
(author)
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Comans, Emile F. I.
(author)
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Hoetjes, Nikie J.
(author)
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Tolboom, Nelleke
(author)
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Langer, Oliver
(author)
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Mueller, Markus
(author)
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Scheltens, Philip
(author)
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Lammertsma, Adriaan A.
(author)
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van Berckel, Bart N. M.
(author)
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Uppsala universitetEnheten för nuklearmedicin och PET
(creator_code:org_t)
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In:Brain: Oxford University Press (OUP)135, s. 181-1890006-89501460-2156
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