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

Nienke M.E. Scheltens*, Kars van der Weijden, Sofie M. Adriaanse, Danielle van Assema, Priscilla P. Oomen, Welmoed A. Krudop, Adriaan A. Lammertsma, Frederik Barkhof, Teddy Koene, Charlotte E. Teunissen, Philip Scheltens, Wiesje M. van der Flier, Yolande A.L. Pijnenburg, Maqsood Yaqub, Rik Ossenkoppele, Bart N.M. van Berckel

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

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.

Original languageEnglish
Pages (from-to)625-632
Number of pages8
JournalNeuroImage: Clinical
Volume19
DOIs
Publication statusPublished - 1 Jan 2018

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