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. 2018 May 22:19:625-632.
doi: 10.1016/j.nicl.2018.05.024. eCollection 2018.

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

Nienke M E Scheltens  1 , Kars van der Weijden  2 , Sofie M Adriaanse  2 , Danielle van Assema  2 , Priscilla P Oomen  3 , Welmoed A Krudop  3 , Adriaan A Lammertsma  2 , Frederik Barkhof  4 , Teddy Koene  5 , Charlotte E Teunissen  6 , Philip Scheltens  3 , Wiesje M van der Flier  7 , Yolande A L Pijnenburg  3 , Maqsood Yaqub  2 , Rik Ossenkoppele  3 , Bart N M van Berckel  2
Affiliations

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

Nienke M E Scheltens et al. Neuroimage Clin. .

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.

Keywords: Alzheimer's disease; Frontotemporal dementia; Hypometabolism; Posterior cingulate cortex; [18F]FDG-PET.

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Figures

Fig. 1
Fig. 1
PCC [18F]FDG uptake visualised in a CN subject (SUVr = 0.948), a bvFTD patient (SUVr = 0.939), and an AD patient (SUVr = 0.768). SUVr were measured using the cerebellum as reference region.
Fig. 2
Fig. 2
Boxplots showing PCC [18F]FDG SUVr in CN, bvFTD, and AD with cerebellum (left panel) and pons (right panel) as reference region. Colours indicate whether PCC hypometabolism was present (dark blue) or absent (light blue) as rated by both readers. Green colours indicate disagreement between readers regarding PCC metabolism; light green indicates normal metabolism, and dark green indicates hypometabolism as rated by BvB, where DvA rated metabolism the other way around. The dotted line corresponds with a cut-off defined using the ROC separating PCC [18F]FDG SUVr in AD versus CN.
Fig. 3
Fig. 3
Receiver operating characteristic separating PCC [18F]FDG SUVr in CN versus AD.
Fig. 4
Fig. 4
Linear regression analyses showed associations between PCC [18F]FDG SUVr and age in AD (pinteraction = 0.047, standardized beta [SE] = 0.010[0.005]), as well as with age at onset of complaints in AD (pinteraction = 0.034, standardized beta[SE] = 0.011[0.055]).
Fig. 5
Fig. 5
Linear regression analyses showed associations between PCC [18F]FDG SUVr and visuospatial functioning in bvFTD patients with PCC hypometabolism (pinteraction = 0.044, eta2 = 0.208, standardized beta[SE] = 0.163[0.075]) using cerebellum as reference region, as well as with memory (pinteraction = 0.002, eta2 = 0.419, standardized beta[SE] = 0.263[0.073]), and CDR (pinteraction = 0.042, eta2 = 0.264, standardized beta[SE] = −0.434[0.104]) using the pons as reference region.
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