Partial volume correction in quantitative amyloid imaging

Su, Yi; Blazey, Tyler; Snyder, Abraham Z.; Raichle, Marcus E.; Marcus, Daniel S.; Ances, Beau M.; Bateman, Randall J.; Cairns, Nigel J.; Aldea, Patricia; Cash, Lisa; Christensen, Jon; Friedrichsen, Karl A.; Hornbeck, Russ C.; Farrar, Angela M.; Owen, Christopher J.; Mayeux, Richard; Brickman, Adam M.; Klunk, William E.; Price, Julie C.; Thompson, Paul M.; Ghetti, Bernardino; Saykin, Andrew J.; Sperling, Reisa A.; Johnson, Keith A.; Schofield, Peter R.; Buckles, Virginia; Morris, John C.; Benzinger, Tammie L.S.

doi:10.1016/j.neuroimage.2014.11.058

Cited by 212 publications

(248 citation statements)

References 43 publications

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“…In work by Drzezga et al on 11 C-Pittsburgh compound B, PVEC had no relevant impact on the apolipoprotein E4 effect in AD patients (19). More recently, Su et al applied PVEC to simulated and human 11 C-Pittsburgh compound B data and demonstrated that PVEC might improve the detection of subtle changes in Ab binding over time (20). Thomas et al used different PVEC approaches on 18 F-flutemetamol PET data; in accordance with our results and depending on the brain region investigated, the modified Müller-Gärtner method yielded different SUVR results in different cohorts (21).…”

Section: Discussionmentioning

confidence: 99%

Partial-Volume Effect Correction Improves Quantitative Analysis of ¹⁸F-Florbetaben β-Amyloid PET Scans

et al. 2015

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Neocortical atrophy reduces PET signal intensity, potentially affecting the diagnostic efficacy of β-amyloid (Aβ) brain PET imaging. This study investigated whether partial-volume effect correction (PVEC), adjusting for this atrophy bias, improves the accuracy of 18 F-florbetaben Aβ PET. Methods: We analyzed 18 F-florbetaben PET and MRI data obtained from 3 cohorts. The first was 10 patients with probable Alzheimer disease (AD) and 10 age-matched healthy controls (HCs), the second was 31 subjects who underwent in vivo imaging and postmortem histopathology for Aβ plaques, and the third was 5 subjects who underwent PET and MRI at baseline and 1 y later. The imaging data were coregistered and segmented. PVEC was performed using the voxel-based modified Müller-Gärtner method (PVELab, SPM8). From the PET data, regional and composite SUV ratios (SUVRs) with and without PVEC were obtained. In the MRI data, mesial temporal lobe atrophy was determined by the Scheltens mesial temporal atrophy scale and gray matter volumes by voxel-based morphometry. Results: In cohort 1, PVEC increased the effect on AD-versus-HC discrimination from a Cohen d value of 1.68 to 2.0 for composite SUVRs and from 0.04 to 1.04 for mesial temporal cortex SUVRs. The PVEC-related increase in mesial temporal cortex SUVR correlated with the Scheltens score (r 5 0.84, P , 0.001), and that of composite SUVR correlated with the composite gray matter volume (r 5 −0.75, P , 0.001). In cohort 2, PVEC increased the correlation coefficient between mesial temporal cortex SUVR and histopathology score for Aβ plaque load from 0.28 (P 5 0.09) to 0.37 (P 5 0.03). In cohort 3, PVEC did not affect the composite SUVR dynamics over time for the Aβ-negative subject. This finding was in contrast to the 4 Aβ-positive subjects, in 2 of whom PVEC changed the composite SUVR dynamics. Conclusion: The influence of PVEC on 18 F-florbetaben PET data is associated with the degree of brain atrophy. Thus, PVEC increases the ability of 18 F-florbetaben PET to discriminate between AD patients and HCs, to detect Aβ plaques in the atrophic mesial temporal cortex, and potentially to evaluate changes in brain Aβ load over time. As such, the use of PVEC should be considered for quantitative 18 F-florbetaben PET scans, especially in assessing patients with brain atrophy.

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Section: Discussionmentioning

confidence: 99%

Partial-Volume Effect Correction Improves Quantitative Analysis of ¹⁸F-Florbetaben β-Amyloid PET Scans

et al. 2015

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“…Deposition of PiB in brain regions of interest was determined using FreeSurfer version 5.1 software (Martinos Center for Biomedical Imaging), 32,34,35 and a standardized uptake value ratio (SUVR) corrected for partial volume effects 36 was calculated for each region of interest. The mean cortical SUVR was calculated from FreeSurfer regions within the prefrontal cortex, precuneus, and temporal cortex.…”

Section: Methodsmentioning

confidence: 99%

Longitudinal Cerebrospinal Fluid Biomarker Changes in Preclinical Alzheimer Disease During Middle Age

et al. 2015

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IMPORTANCE Individuals in the presymptomatic stage of Alzheimer disease (AD) are increasingly being targeted for AD secondary prevention trials. How early during the normal life span underlying AD pathologies begin to develop, their patterns of change over time, and their relationship with future cognitive decline remain to be determined. OBJECTIVE To characterize the within-person trajectories of cerebrospinal fluid (CSF) biomarkers of AD over time and their association with changes in brain amyloid deposition and cognitive decline in cognitively normal middle-aged individuals. DESIGN, SETTING, AND PARTICIPANTS As part of a cohort study, cognitively normal (Clinical Dementia Rating [CDR] of 0) middle-aged research volunteers (n = 169) enrolled in the Adult Children Study at Washington University, St Louis, Missouri, had undergone serial CSF collection and longitudinal clinical assessment (mean, 6 years; range, 0.91-11.3 years) at 3-year intervals at the time of analysis, between January 2003 and November 2013. A subset (n = 74) had also undergone longitudinal amyloid positron emission tomographic imaging with Pittsburgh compound B (PiB) in the same period. Serial CSF samples were analyzed for β-amyloid 40 ( Aβ40), Aβ42, total tau, tau phosphorylated at threonine 181 (P-tau 181 ), visinin-like protein 1 (VILIP-1), and chitinase-3-like protein 1 (YKL-40). Within-person measures were plotted according to age and AD risk defined by APOE genotype (ε4 carriers vs noncarriers). Linear mixed models were used to compare estimated biomarker slopes among middle-age bins at baseline (early, 45-54 years; mid, 55-64 years; late, 65-74 years) and between risk groups. Within-person changes in CSF biomarkers were also compared with changes in cortical PiB binding and progression to a CDR higher than 0 at follow-up. MAIN OUTCOMES AND MEASURESChanges in Aβ40, Aβ42, total tau, P-tau 181 , VILIP-1, and YKL-40 and, in a subset of participants, changes in cortical PiB binding.RESULTS While there were no consistent longitudinal patterns in Aβ40 (P = .001-.97), longitudinal reductions in Aβ42 were observed in some individuals as early as early middle age (P Յ .05) and low Aβ42 levels were associated with the development of cortical PiB-positive amyloid plaques (area under receiver operating characteristic curve = 0.9352; 95% CI, 0.8895-0.9808), especially in mid middle age (P < .001). Markers of neuronal injury (total tau, P-tau 181 , and VILIP-1) dramatically increased in some individuals in mid and late middle age (P Յ .02), whereas the neuroinflammation marker YKL-40 increased consistently throughout middle age (P Յ .003). These patterns were more apparent in at-risk ε4 carriers (Aβ42 in an allele dose-dependent manner) and appeared to be associated with future cognitive deficits as determined by CDR. CONCLUSIONS AND RELEVANCELongitudinal CSF biomarker patterns consistent with AD are first detectable during early middle age and are associated with later amyloid positivity and cognitive decline. Such measures may be useful for targeti...

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“…The SUVR of the prefrontal cortex, temporal lobe, gyrus rectus and precuneus were averaged to calculate a total cortex SUVR. An SUVR of 1·3 was used to stratify the cohort based on amyloid positivity (PiB- < 1·3, PiB+ ≥ 1·3) [20]. …”

Section: Methodsmentioning

confidence: 99%

Habitual exercise levels are associated with cerebral amyloid load in presymptomatic autosomal dominant Alzheimer's disease

Brown

Sohrabi

Taddei

et al. 2017

Alzheimer's & Dementia

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Introduction The objective of this study was to evaluate the relationship between self-reported exercise levels and Alzheimer's disease biomarkers, in a cohort of autosomal dominant Alzheimer's disease (ADAD) mutation carriers. Methods In 139 pre-symptomatic mutation carriers from the Dominantly Inherited Alzheimer Network, the relationship between self-reported exercise levels and brain amyloid load, CSF Aβ42 and tau levels was evaluated using linear regression. Results No differences in brain amyloid load, CSF Aβ42 or tau were observed between low and high exercise groups. Nevertheless, when examining only those already accumulating AD pathology (i.e. amyloid positive), low exercisers had higher mean levels of brain amyloid than high exercisers. Furthermore, the interaction between exercise*estimated years from expected symptom onset was a significant predictor of brain amyloid levels. Discussion Our findings indicate a relationship exists between self-reported exercise levels and brain amyloid in ADAD mutation carriers.

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Partial volume correction in quantitative amyloid imaging

Cited by 212 publications

References 43 publications

Partial-Volume Effect Correction Improves Quantitative Analysis of ¹⁸F-Florbetaben β-Amyloid PET Scans

Partial-Volume Effect Correction Improves Quantitative Analysis of ¹⁸F-Florbetaben β-Amyloid PET Scans

Longitudinal Cerebrospinal Fluid Biomarker Changes in Preclinical Alzheimer Disease During Middle Age

Habitual exercise levels are associated with cerebral amyloid load in presymptomatic autosomal dominant Alzheimer's disease

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Partial volume correction in quantitative amyloid imaging

Cited by 212 publications

References 43 publications

Partial-Volume Effect Correction Improves Quantitative Analysis of 18F-Florbetaben β-Amyloid PET Scans

Partial-Volume Effect Correction Improves Quantitative Analysis of 18F-Florbetaben β-Amyloid PET Scans

Longitudinal Cerebrospinal Fluid Biomarker Changes in Preclinical Alzheimer Disease During Middle Age

Habitual exercise levels are associated with cerebral amyloid load in presymptomatic autosomal dominant Alzheimer's disease

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Partial-Volume Effect Correction Improves Quantitative Analysis of ¹⁸F-Florbetaben β-Amyloid PET Scans

Partial-Volume Effect Correction Improves Quantitative Analysis of ¹⁸F-Florbetaben β-Amyloid PET Scans