FDG-PET hypermetabolism is associated with higher tau-PET in mild cognitive impairment at low amyloid-PET levels
- PDF / 2,846,790 Bytes
- 12 Pages / 595.276 x 790.866 pts Page_size
- 52 Downloads / 188 Views
(2020) 12:133
RESEARCH
Open Access
FDG-PET hypermetabolism is associated with higher tau-PET in mild cognitive impairment at low amyloid-PET levels Anna Rubinski1, Nicolai Franzmeier1, Julia Neitzel1, Michael Ewers1,2* Initiative (ADNI)
and the Alzheimer’s Disease Neuroimaging
Abstract Background: FDG-PET hypermetabolism can be observed in mild cognitive impairment (MCI), but the link to primary pathologies of Alzheimer’s diseases (AD) including amyloid and tau is unclear. Methods: Using voxel-based regression, we assessed local interactions between amyloid- and tau-PET on spatially matched FDG-PET in 72 MCI patients. Control groups included cerebrospinal fluid biomarker characterized cognitively normal (CN, n = 70) and AD dementia subjects (n = 95). Results: In MCI, significant amyloid-PET by tau-PET interactions were found in frontal, lateral temporal, and posterior parietal regions, where higher local tau-PET was associated with higher spatially corresponding FDG-PET at low levels of local amyloid-PET. FDG-PET in brain regions with a significant local amyloid- by tau-PET interaction was higher compared to that in CN and AD dementia and associated with lower episodic memory. Conclusion: Higher tau-PET in the presence of low amyloid-PET is associated with abnormally increased glucose metabolism that is accompanied by episodic memory impairment. Keywords: FDG-PET, Hypermetabolism, Tau-PET, Amyloid-PET, Hyperactivation, Mild cognitive impairment
Introduction In Alzheimer’s disease (AD), alterations in glucose metabolism as assessed by [18F]fluorodeoxyglucose positron emission tomography (FDG-PET) are a common pathological hallmark [1]. Specifically, FDG-PET hypometabolism within temporoparietal regions is commonly observed in AD dementia and earlier AD stages, including in amyloid-positive mild cognitive impairment (MCI; i.e., prodromal AD) [2] and cognitively normal (CN) elderly at genetic risk of AD [3]. However, FDG-PET metabolism shows complex changes during the course of * Correspondence: [email protected] 1 Institute for Stroke and Dementia Research, Klinikum der Universität München, Ludwig-Maximilians-Universität LMU, Feodor-Lynen-Straße 17, 81377 Munich, Germany 2 German Center for Neurodegenerative Diseases, Munich, Germany
AD, where not only reductions but also increases in FDG-PET metabolism have been reported across CN amyloid-positive subjects [4] and subjects at genetic risk of AD [5, 6] and MCI [7]. Thus, clinical staging of cognitive symptoms does not correspond to FDG-PET alterations in a straightforward manner. Studies using amyloid- and tau-PET imaging suggest that these pathologies are important predictors of regional FDG-PET alterations. For amyloid-PET, elevated global levels of amyloid-PET have been associated with reduced FDG-PET in both AD dementia [8] and MCI [9]. However, increased FDG-PET has also been observed in association with elevated amyloid-PET [4]. Furthermore, there is a poor regional match between amyloid-PET and FDG-PET in typical [10] and atypical AD [11
Data Loading...
