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Case Reports
. 2015 Aug 26:15:152.
doi: 10.1186/s12883-015-0410-5.

Dissociation of amyloid biomarkers in PET and CSF in Alzheimer's disease: a case report

Matthias L Schroeter  1   2   3   4 , Solveig Tiepolt  5 , Anke Marschhauser  6 , Angelika Thöne-Otto  7 , Karl-Titus Hoffmann  8 , Henryk Barthel  9 , Hellmuth Obrig  10   11 , Osama Sabri  12
Affiliations
Case Reports

Dissociation of amyloid biomarkers in PET and CSF in Alzheimer's disease: a case report

Matthias L Schroeter et al. BMC Neurol. .

Abstract

Background: Recently, biomarkers have been suggested to be incorporated into diagnostic criteria for Alzheimer's disease (AD). Regarding disease-specific brain amyloid-beta deposition these comprise low amyloid-beta 1-42 in cerebrospinal fluid (CSF) and positive positron emission tomography (PET) amyloid imaging, while neuronal degeneration is evidenced by high total and phosphorylated tau levels in CSF (t-/p-tau), regional hypometabolism ([(18)F]fluorodeoxyglucose PET, FDG-PET) and characteristic atrophy-patterns (magnetic resonance imaging, MRI).

Case presentation: Here we present a case of clinically and biomarker supported AD (CSF t-/p-tau, MRI, FDG-PET) in a 59-year-old Caucasian man in whom indicators of amyloid-beta deposition dissociated between CSF parameters and the respective PET imaging.

Conclusions: Such cases highlight the necessity to better understand potential dissociations between PET and CSF data for amyloid-beta biomarkers, because they are currently considered interchangeably valid with regard to in-vivo evidence for AD pathology. This is more important since amyloid deposition markers can be considered a very first prognostic indicator of imminent AD, prior to neurodegenerative biomarkers and cognitive symptoms. The case illustrates the need for further longitudinal data on potential dissociations of AD biomarkers to devise recommendations for their better prognostic and diagnostic interpretation in the future.

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Figures

Fig. 1
Fig. 1
Imaging biomarkers for Alzheimer’s disease. Atrophy was evident in magnetic resonance imaging (MRI) in temporal/hippocampal regions in T1 (a) and T2 (b) sequence, and in parietal cortex in T1 (c). Single white matter lesions were detected in fast fluid-attenuated inversion recovery (FLAIR) images (d). Amyloid positron emission tomography (PET) with [18F]florbetaben did not show specific binding in the neocortical gray matter (e), although hypometabolism was detected in bilateral parietotemporal and posterior cingluate cortices with [18F]fluorodeoxyglucose-PET (f). Finally, we evaluated statistical deviation of tracer uptake from a normal control group including 94 (amyloid) or 25 (glucose) normal subjects with the Hermes Brass Software. Z score map of the [18F]florbetaben PET (g) did not show relevant (z score > 2.5) cortical tracer uptake increase, whereas the z score map of [18F]fluorodeoxyglucose-PET (h) showed relevant (z score > 2.5) tracer uptake reduction in bilateral parietotemporal regions and posterior cingulate cortices
See this image and copyright information in PMC

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