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Ann Neurol. 2015 Feb;77(2):338-42. doi: 10.1002/ana.24321. Epub 2014 Dec 17.

Tau, amyloid, and hypometabolism in a patient with posterior cortical atrophy.

Author information

1
Memory and Aging Center, University of California, San Francisco, San Francisco; Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley.

Abstract

Determining the relative contribution of amyloid plaques and neurofibrillary tangles to brain dysfunction in Alzheimer disease is critical for therapeutic approaches, but until recently could only be assessed at autopsy. We report a patient with posterior cortical atrophy (visual variant of Alzheimer disease) who was studied using the novel tau tracer [(18) F]AV-1451 in conjunction with [(11) C]Pittsburgh compound B (PIB; amyloid) and [(18) F]fluorodeoxyglucose (FDG) positron emission tomography. Whereas [(11) C]PIB bound throughout association neocortex, [(18) F]AV-1451 was selectively retained in posterior brain regions that were affected clinically and showed markedly reduced [(18) F]FDG uptake. This provides preliminary in vivo evidence that tau is more closely linked to hypometabolism and symptomatology than amyloid.

PMID:
25448043
PMCID:
PMC4382124
DOI:
10.1002/ana.24321
[Indexed for MEDLINE]
Free PMC Article

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