Abstract
Purpose18F-APN-1607 is a novel tau positron emission tomography (PET) tracer characterized with high binding affinity for 3− and 4-repeat tau deposits. The aim was to analyze the spatial distribution of 18F-APN-1607 PET imaging in Alzheimer’s disease (AD) subjects with different stages and to investigate the relationship between the change of tau deposition and overall disease progression.MethodsWe retrospectively analyzed the 18F-APN-1607 PET imaging of 31 subjects with clinically and imaging defined as AD. According to the Mini-Mental State Examination (MMSE) score, patients were divided into three groups, namely, mild (≥21, n = 7), moderate (10–20, n = 16), and severe (≤9, n = 8). PET imaging was segmented to 70 regions of interest (ROIs) and extracted the standard uptake value (SUV) of each ROI. SUV ratio (SUVR) was calculated from the ratio of SUV in different brain regions to the cerebellar cortex. The regions were defined as positive and negative with unsupervised cluster analysis according to SUVR. The SUVRs of each region were compared among groups with the one-way ANOVA or Kruskal–Wallis H test. Furthermore, the correlations between MMSE score and regional SUVR were calculated with Pearson or Spearman correlation analysis.ResultsThere were no significant differences among groups in gender (χ2 = 3.814, P = 0.161), age of onset (P = 0.170), age (P = 0.109), and education level (P = 0.065). With the disease progression, the 18F-APN-1607 PET imaging showed the spread of tau deposition from the hippocampus, posterior cingulate gyrus (PCG), and lateral temporal cortex (LTC) to the parietal and occipital lobes, and finally to the frontal lobe. Between the mild and moderate groups, the main brain areas with significant differences in 18F-APN-1607 uptake were supplementary motor area (SMA), cuneus, precuneus, occipital lobule, paracentral lobule, right angular gyrus, and parietal, which could be used for early disease progression assessment (P < 0.05). There were significant differences in the frontal lobe, right temporal lobe, and fusiform gyrus between the moderate and severe groups, which might be suitable for the late-stage disease progression assessment (P < 0.05).Conclusion18F-APN-1607 PET may serve as an effective imaging marker for visualizing the change pattern of tau protein deposition in AD patients, and its uptake level in certain brain regions is closely related to the severity of cognitive impairment. These indicate the potential of 18F-APN-1607 PET for the in vivo evaluation of the progression of AD.
Highlights
Alzheimer’s disease (AD) is the most common cause of dementia in elderly people, which is mainly manifested as learning and memory impairment, aphasia, agnosia, impairment of visual and spatial skills, change in abstract thinking, and gradual impairment of daily functions (Longhe, 2020)
Our results showed that with the disease progression, the 18FAPN-1607 positron emission tomography (PET) imaging showed the spread of tau deposition from the hippocampus, posterior cingulate gyrus (PCG), and lateral temporal cortex (LTC) to the parietal and occipital lobes, and to the frontal lobe
These suggested that 18F-APN-1607 PET may serve as an effective imaging marker for visualizing the change of tau protein deposition in AD patients, and its uptake pattern in different brain regions may relate to the progress of cognitive impairment
Summary
Alzheimer’s disease (AD) is the most common cause of dementia in elderly people, which is mainly manifested as learning and memory impairment, aphasia, agnosia, impairment of visual and spatial skills, change in abstract thinking, and gradual impairment of daily functions (Longhe, 2020). The details of the pathological mechanism of AD were not completely clear, the main pathological features were extracellular plaques composed of Aβ-amyloid (Aβ) and intracellular neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau protein. Autopsy studies had shown that, compared with Aβ plaque density, NFT was believed to be more directly related to neuron loss and synaptic dysfunction and more closely related to AD cognitive impairment (Hadjichrysanthou et al, 2020). National Institute of Aging, Alzheimer’s Association (NIA-AA) had made it clear that, regardless of cognitive symptoms, AD could be determined only based on abnormal Aβ and tau protein deposition (Jack et al, 2018)
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