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Hypometabolism of the posterior cingulate cortex is not restricted to Alzheimer's disease.

Abstract：

:When differential diagnosis of dementia includes both Alzheimer's disease (AD) and the behavioural variant of frontotemporal dementia (bvFTD), distribution of cerebral glucose metabolism as measured using [18F]‑2‑fluoro‑2‑deoxy‑d‑glucose positron emission tomography ([18F]FDG-PET) may be helpful. One important clue for differentiation is the presence of hypometabolism in the posterior cingulate cortex (PCC), usually associated with AD. PCC hypometabolism however, could also be present in bvFTD. Therefore, the specificity of PCC hypometabolism was examined. Based on visual reading PCC hypometabolism was present in 69-73/81 probable AD patients, in 10-16/33 probable bvFTD patients, and in 0-1/22 cognitive normal (CN) subjects. Findings were validated using a PCC to reference tissue [18F]FDG standard uptake value ratio (SUVr) cut-off, which was derived from the receiver operating characteristic (ROC) separating probable AD from CN, resulting in 9-14/33 bvFTD patients having PCC hypometabolism, depending on the reference tissue used. In conclusion, PCC hypometabolism is not restricted to AD.

journal_name

Neuroimage Clin

journal_title

NeuroImage. Clinical

authors

Scheltens NME,van der Weijden K,Adriaanse SM,van Assema D,Oomen PP,Krudop WA,Lammertsma AA,Barkhof F,Koene T,Teunissen CE,Scheltens P,van der Flier WM,Pijnenburg YAL,Yaqub M,Ossenkoppele R,van Berckel BNM

doi

10.1016/j.nicl.2018.05.024

subject

Has Abstract

pub_date

2018-05-22 00:00:00

pages

625-632

issn

2213-1582

pii

S2213-1582(18)30170-0

journal_volume

19

pub_type

杂志文章

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