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No evidence for additional blood-brain barrier P-glycoprotein dysfunction in Alzheimer's disease patients with microbleeds

van Assema, Danielle M. E. (author)
Goos, Jeroen D. C. (author)
van der Flier, Wiesje M. (author)
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Lubberink, Mark (author)
Uppsala universitet,Enheten för nuklearmedicin och PET
Boellaard, Ronald (author)
Windhorst, Albert D. (author)
Scheltens, Philip (author)
Lammertsma, Adriaan A. (author)
van Berckel, Bart N. M. (author)
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 (creator_code:org_t)
2012-05-16
2012
English.
In: Journal of Cerebral Blood Flow and Metabolism. - : SAGE Publications. - 0271-678X .- 1559-7016. ; 32:8, s. 1468-1471
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • Decreased blood-brain barrier P-glycoprotein (Pgp) function has been shown in Alzheimer's disease (AD) patients using positron emission tomography (PET) with the radiotracer (R)-[C-11] verapamil. Decreased Pgp function has also been hypothesized to promote cerebral amyloid angiopathy (CAA) development. Here, we used PET and (R)-[C-11] verapamil to assess Pgp function in eighteen AD patients, of which six had microbleeds (MBs), presumably reflecting underlying CAA. No differences were found in binding potential and nonspecific volume of distribution of (R)-[C-11] verapamil between patient groups. These results provide no evidence for additional Pgp dysfunction in AD patients with MBs.

Keyword

Alzheimer's disease
blood-brain barrier
cerebral amyloid angiopathy
P-glycoprotein
positron emission tomography
(R)-[C-11]verapamil

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art (subject category)

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