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Abstract
BackgroundTo compare the neocortical amyloid loads among cognitively normal (CN), amnestic mild cognitive impairment (aMCI), and Alzheimer's disease (AD) subjects with [18F]AV-45 positron emission tomography (PET).Materials and Methods[18F]AV-45 PET was performed in 11 CN, 13 aMCI, and 12 AD subjects to compare the cerebral cortex-to-whole cerebellum standard uptake value ratios (SUVRs) of global and individual volumes of interest (VOIs) cerebral cortex. The correlation between global cortical [18F]AV-45 SUVRs and Mini-Mental State Examination (MMSE) scores was analyzed.ResultsThe global cortical [18F]AV-45 SUVRs were significantly different among the CN (1.08±0.08), aMCI (1.27±0.06), and AD groups (1.34±0.13) (p = 0.0003) with amyloidosis positivity rates of 9%, 62%, and 92% in the three groups respectively. Compared to CN subjects, AD subjects had higher SUVRs in the global cortical, precuneus, frontal, parietal, occipital, temporal, and posterior cingulate areas; while aMCI subjects had higher values in the global cortical, precuneus, frontal, occipital and posterior cingulate areas. There were negative correlations of MMSE scores with SUVRs in the global cortical, precuneus, frontal, parietal, occipital, temporal, posterior cingulate and anterior cingulate areas on a combined subject pool of the three groups after age and education attainment adjustment.ConclusionsAmyloid deposition occurs relatively early in precuneus, frontal and posterior cingulate in aMCI subjects. Higher [18F]AV-45 accumulation is present in parietal, occipital and temporal gyri in AD subjects compared to the aMCI group. Significant correlation between MMSE scores and [18F]AV-45 SUVRs can be observed among CN, aMCI and AD subjects.
Highlights
Alzheimer’s disease (AD) is the most common cause of dementia and leads to progressive dysfunctions in memory and other cognitive domains
The standard uptake value ratios (SUVRs) of the global cortical, precuneus, frontal, occipital and posterior cingulate areas were higher in amnestic mild cognitive impairment (aMCI) subjects than cognitively normal (CN) subjects
There were varying degrees of [18F]AV-45 retention in CN, aMCI negative for cerebral amyloidosis (aMCI (2)), aMCI positive for cerebral amyloidosis (aMCI (+)), and AD subjects, whose patterns closely followed the amyloid deposition distribution observed in post mortem brain tissue (Figure 2) [26]
Summary
Alzheimer’s disease (AD) is the most common cause of dementia and leads to progressive dysfunctions in memory and other cognitive domains. The diagnosis of AD is hampered by a lack of noninvasive biomarkers. 67% of dementia patients with mild clinical symptoms may not be diagnosed by physicians [1]. The most widely accepted pathogeneses of AD include increased production or impaired clearance of amyloid-beta oligomers, resulting in excessive fibrillary amyloid plaque accumulation in the brain. The accumulation of amyloid plaques may precede the diagnosis of AD by 10 years [2]. A reliable biomarker for determination of amyloid plaque aggregates could facilitate an early diagnosis and treatment of AD. To compare the neocortical amyloid loads among cognitively normal (CN), amnestic mild cognitive impairment (aMCI), and Alzheimer’s disease (AD) subjects with [18F]AV-45 positron emission tomography (PET)
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