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Meeting ReportNeurosciences Track

Amyloid accumulation, glucose hypometabolism, and gray matter atrophy in Down syndrome

Patrick Lao, Ben Handen, Tobey Betthauser, Julie Price, William Klunk, Peter Bulova, Sigan Hartley, Reginah Hardison, Rameshwari Tumuluru, Dhanabalan Murali, Chester Mathis, Annie Cohen, Todd Barnhart, Dana Tudorascu, Darlynne Devenny, Sterling Johnson and Bradley Christian
Journal of Nuclear Medicine May 2017, 58 (supplement 1) 557;
Patrick Lao
6University of Wisconsin at Madison Madison WI United States
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Ben Handen
4University of Pittsburgh Pittsburgh PA United States
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Tobey Betthauser
7University of Wisconsin-Madison Madison WI United States
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Julie Price
2Massachusetts General Hospital Boston MA United States
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William Klunk
4University of Pittsburgh Pittsburgh PA United States
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Peter Bulova
8UPMC Pittsburgh PA United States
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Sigan Hartley
6University of Wisconsin at Madison Madison WI United States
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Reginah Hardison
4University of Pittsburgh Pittsburgh PA United States
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Rameshwari Tumuluru
11011 Bingham Street PGH PA United States
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Dhanabalan Murali
5University of Wisconsin Madison WI United States
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Chester Mathis
4University of Pittsburgh Pittsburgh PA United States
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Annie Cohen
4University of Pittsburgh Pittsburgh PA United States
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Todd Barnhart
5University of Wisconsin Madison WI United States
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Dana Tudorascu
4University of Pittsburgh Pittsburgh PA United States
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Darlynne Devenny
3New York State Institute for Basic Research in Developmental Disabilities New York City NY United States
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Sterling Johnson
7University of Wisconsin-Madison Madison WI United States
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Bradley Christian
7University of Wisconsin-Madison Madison WI United States
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Abstract

557

Objectives: Amyloid-β plaques, cerebral hypometabolism, and gray matter (GM) atrophy are common biomarkers for Alzheimer’s disease (AD) pathology. The aim of this work was to use functional and structural imaging to provide insight into the association between these AD biomarkers in the Down syndrome (DS) population, which is genetically predisposed to early amyloid-β accumulation and AD.

Methods: Twenty-three non-demented adults (12M,11F; 38.6±7.0yrs) with DS underwent [11C]PiB scan and a subsequent [18F]FDG scan (124.7±102.6 days after), as well as T1 and T2 MRIs at each visit. Parametric standard uptake value ratios (SUVRs) were calculated for PiB (50-70 min) and FDG (40-60 min) using cerebellar gray matter as the reference region. Parametric GM volume images were estimated from a multispectral tissue-type segmentation (Matlab2015, SPM12). Parametric images were spatially normalized using a study-specific PET template and analyzed in MNI space. Biological parametric mapping (BPM; MATLAB2011a, SPM5) was used to investigate associations between PiB and FDG SUVR images, as well as GM volume images. Common covariates, including age, sex, cognitive function, and APOE4 allele, were investigated in SPM12 (cluster size >1000 voxels, αuncorrected=0.001).

Results: PiB and FDG SUVR were negatively associated in the precuneus and left parietal cortex, while PiB or FDG SUVR were not associated with GM volume. BPM results did not survive correction for age, but survived separate correction for sex, cognitive function, and APOE4 in this non-demented cohort of adults with DS. SPM analysis showed a positive association between PiB SUVR and age in the anterior cingulate, frontal cortex, parietal cortex, precuneus, striatum, and temporal cortex. FDG SUVR was negatively associated with age in the precuneus, right parietal and temporal cortex, and right thalamus. GM was negatively associated with age in the frontal cortex.

Conclusion: Imaging in the non-demented DS population demonstrates AD-like neuropathology, such as early amyloid accumulation and glucose hypometabolism. While, the amyloid accumulation and glucose hypometabolism were correlated in regions consistent with AD, the GM atrophy occurred in frontal cortex, which is typically spared until later in the AD process. Therefore, the GM atrophy beginning in the frontal cortex may reflect the DS phenotype. Research Support: R01 AG031110, U54 HD090256, U01 AG051406

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Journal of Nuclear Medicine
Vol. 58, Issue supplement 1
May 1, 2017
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Amyloid accumulation, glucose hypometabolism, and gray matter atrophy in Down syndrome
Patrick Lao, Ben Handen, Tobey Betthauser, Julie Price, William Klunk, Peter Bulova, Sigan Hartley, Reginah Hardison, Rameshwari Tumuluru, Dhanabalan Murali, Chester Mathis, Annie Cohen, Todd Barnhart, Dana Tudorascu, Darlynne Devenny, Sterling Johnson, Bradley Christian
Journal of Nuclear Medicine May 2017, 58 (supplement 1) 557;

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Amyloid accumulation, glucose hypometabolism, and gray matter atrophy in Down syndrome
Patrick Lao, Ben Handen, Tobey Betthauser, Julie Price, William Klunk, Peter Bulova, Sigan Hartley, Reginah Hardison, Rameshwari Tumuluru, Dhanabalan Murali, Chester Mathis, Annie Cohen, Todd Barnhart, Dana Tudorascu, Darlynne Devenny, Sterling Johnson, Bradley Christian
Journal of Nuclear Medicine May 2017, 58 (supplement 1) 557;
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