Abstract
In vivo quantification of β-amyloid deposition using positron emission tomography is emerging as an important procedure for the early diagnosis of the Alzheimer's disease and is likely to play an important role in upcoming clinical trials of disease modifying agents. However, many groups use manually defined regions, which are non-standard across imaging centers. Analyses often are limited to a handful of regions because of the labor-intensive nature of manual region drawing. In this study, we developed an automatic image quantification protocol based on FreeSurfer, an automated whole brain segmentation tool, for quantitative analysis of amyloid images. Standard manual tracing and FreeSurfer-based analyses were performed in 77 participants including 67 cognitively normal individuals and 10 individuals with early Alzheimer's disease. The manual and FreeSurfer approaches yielded nearly identical estimates of amyloid burden (intraclass correlation = 0.98) as assessed by the mean cortical binding potential. An MRI test-retest study demonstrated excellent reliability of FreeSurfer based regional amyloid burden measurements. The FreeSurfer-based analysis also revealed that the majority of cerebral cortical regions accumulate amyloid in parallel, with slope of accumulation being the primary difference between regions.
Highlights
The prevalence of Alzheimer’s disease (AD) is expected to increase dramatically worldwide within the 50 years [1]
We develop an automated, regional, quantitative amyloid imaging analysis protocol using FreeSurfer (Martinos Center for Biomedical Imaging, Charlestown, Massachusetts). We demonstrate that this protocol generates global amyloid deposition measurements comparable to results obtained with conventional hand drawn regions
Participants Seventy-seven individuals (G1) aged 48 to 90 years old were selected from a larger population enrolled at the Washington University Knight Alzheimer’s Disease Research Center (KADRC) in longitudinal studies of memory and aging
Summary
The prevalence of Alzheimer’s disease (AD) is expected to increase dramatically worldwide within the 50 years [1]. The future success of disease-modifying therapies will depend on accurate early diagnosis before the onset of clinical symptoms [2,3,4]. Amyloid-beta (Ab) plaque deposition is a hallmark of AD [5,6]. With the development of positron emission tomography (PET) tracers with high affinity for Ab plaques, such as 11CPittsburgh Compound B (PiB), it is possible to quantify neuropathology that was previously detectable only by postmortem examination [7]. PET enables in vivo visualization of AD pathology and allows for a broad range of metabolic processes to be assessed in preclinical and clinical AD. It is critical to quantify the Ab burden accurately and robustly, to further our understanding of disease mechanisms and to develop early diagnostic techniques
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