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CSF tau phosphorylated at threonine 181 (p-tau181) is a widely used biomarker for Alzheimer's disease (AD) and has recently been regarded to reflect amyloid-beta and/or p-tau deposition in the AD brain. Neuronal intranuclear inclusion disease (NIID) is a neurodegenerative disease characterized by intranuclear inclusions in neurons, glial cells, and other somatic cells. Symptoms include dementia, neuropathy, and others. CSF biomarkers were not reported. The objective of this study was to investigate whether CSF biomarkers including p-tau181 are altered in patients with NIID.This was a retrospective observational study. CSF concentrations of p-tau181, total tau, amyloid-beta 1-42 (Aβ42), monoamine metabolites homovanillic acid (HVA), and 5-hydroxyindole acetic acid (5-HIAA) were compared between 12 patients with NIID, 120 patients with Alzheimer's clinical syndrome biologically confirmed based on CSF biomarker profiles, and patients clinically diagnosed with other neurocognitive disorders (dementia with Lewy bodies [DLB], 24; frontotemporal dementia [FTD], 13; progressive supranuclear palsy [PSP], 21; and corticobasal syndrome [CBS], 13). Amyloid PET using Pittsburgh compound B (PiB) was performed in six NIID patients.The mean age of patients with NIID, AD, DLB, FTD, PSP, and CBS were 71.3, 74.6, 76.8, 70.2, 75.5, and 71.9 years old, respectively. CSF p-tau181 was significantly higher in NIID (72.7 ± 24.8 pg/mL) compared to DLB, PSP, and CBS and was comparable between NIID and AD. CSF p-tau181 was above the cutoff value (50.0 pg/mL) in 11 of 12 NIID patients (91.7%). Within these patients, only two patients showed decreased CSF Aβ42, and these patients showed negative or mild local accumulation in PiB PET, respectively. PiB PET scans were negative in the remaining 4 patients tested. The proportion of patients with increased CSF p-tau181 and normal Aβ42 (A-T+) was significantly higher in NIID (75%) compared to DLB, PSP, and CBS (4.2%, 4.8%, and 7.7%, respectively). CSF HVA and 5-HIAA concentrations were significantly higher in patients with NIID compared to disease controls.CSF p-tau181 was increased in patients with NIID without amyloid accumulation. Although the deposition of p-tau has not been reported in NIID brains, molecular mechanism of tau phosphorylation or secretion of p-tau may be altered in NIID.

Objective: 5-(1-(2-[18F]fluoroethoxy))-[3-(6,7-dimethoxy-3,4-dihydro-1H-isoquinolin-2-yl)-propyl]-5,6,7,8-tetrahydronaphthalen ([18F]MC225) is a selective substrate for P-glycoprotein (P-gp), possessing suitable properties for measuring overexpression of P-gp in the brain. This is the first-in-human study to examine safety, radiation dosimetry and P-gp function at the blood-brain barrier (BBB) of [18F]MC225 in healthy subjects.Methods: [18F]MC225 biodistribution and dosimetry were determined in 3 healthy male subjects, using serial 2 h and intermittent 4 and 6 h whole-body PET scans acquired after [18F]MC225 injection. Dynamic [18F]MC225 brain PET (90 min) was obtained in 5 healthy male subjects. Arterial blood was sampled at various time intervals during scanning and the fraction of unchanged [18F]MC225 in plasma was determined. T1-weighted MRI was performed for anatomical coregistration. Total distribution volume (VT) was estimated using 1- and 2-tissue-compartment models (1-TCM and 2-TCM, respectively). VT was also estimated using the Logan graphical method (Logan plot) (t* = 20 min). Surrogate parameters without blood sampling (area-under the curve [AUC] of regional time-activity curves [TACs] and negative slope of calculated TACs) were compared with the VT values.Results: No serious adverse events occurred throughout the study period. Although biodistribution implied hepatobiliary excretion, secretion of radioactivity from liver to small intestine through the gallbladder was very slow. Total renal excreted radioactivity recovered during 6 h after injection was < 2%ID. Absorbed dose was the highest in the pancreas (mean ± SD, 203 ± 45 μGy/MBq) followed by the liver (83 ± 11 μGy/MBq). Mean effective dose with and without urination was 17 ± 1 μSv/MBq. [18F]MC225 readily entered the brain, distributing homogeneously in grey matter regions. 2-TCM provided lower Akaike information criterion scores than did 1-TCM. VT estimated by Logan plot was well correlated with that of 2-TCM (r2 > 0.9). AUCs of TACs were positively correlated with VT (2-TCM) values (r2: AUC0-60 min = 0.61, AUC0-30 min = 0.62, AUC30-60 min = 0.59, p < 0.0001). Negative slope of SUV TACs was negatively correlated with VT (2-TCM) values (r2 = 0.53, p < 0.0001).Conclusions: This initial evaluation indicated that [18F]MC225 is a suitable and safe PET tracer for measuring P-gp function at the BBB.Keywords: Blood–Brain barrier; Dosimetry; First-in-human; P-glycoprotein; Positron emission tomography.

A 52-year-old woman complained of upper respiratory symptoms and subsequently developed Wallenberg syndrome. Chest CT and brain MRI revealed multiple nodular lesions in the lungs and brain. She was pathologically diagnosed with low-grade lymphomatoid granulomatosis by lung biopsy. Brain PET examinations using 11C-methionine, 18F-FDG, and 18F-THK5351 were performed. Uptake of 11C-methionine and 18F-FDG was slightly increased in some lesions, likely reflecting the degree of inflammatory cell infiltration. 18F-THK5351 uptake was significantly increased in all lesions, likely reflecting the degree of reactive astrogliosis. This case illustrates the utility of PET studies for diagnosing lymphomatoid granulomatosis and provides insight into its pathophysiology.

Background and purpose Little evidence exists on the role of type 1 metabotropic glutamate receptor (mGluR1) in the pathophysiology of Alzheimer's disease (AD), although mGluR1 may be involved in the regulation of neuronal excitability and synaptic plasticity. We have recently reported that mGluR1 availability in the early stage of AD is equivalent to that in healthy subjects. This study aimed to address whether mGluR1 availability changes with the progression of AD. Methods Eight patients with AD (79.1 ± 4.6 years) underwent a total of two positron emission tomography (PET) examinations using the mGluR1 radioligand during the early-to-middle stages of AD. The mean interval was 2.8 years. Volumes-of-interest were placed on the frontal, parietal, and temporal cortices, hippocampus, anterior and posterior lobes, and vermis in the cerebellum. The binding potential (BPND ) was calculated to estimate mGluR1 availability, applying partial volume correction to the BPND values. Results No significant difference was observed in BPND values between the first and second PET examinations in the frontal cortex (p = 0.94), parietal cortex (p = 0.67), temporal cortex (p = 0.20), hippocampus (p = 0.17), anterior lobe (p = 0.73), posterior lobe (p = 0.21), and vermis (p = 0.22). Conclusion This study suggests that mGluR1 availability is unchanged in the follow-up period of a few years during the early-to-middle stages of AD.

Background and ObjectivesCSF tau phosphorylated at threonine 181 (p-tau181) is a widely used biomarker for Alzheimer’s disease (AD) and has recently been regarded to reflect amyloid-beta (Aβ) and/or p-tau deposition in the AD brain. Although it is important to know how this biomarker reacts in other neurocognitive diseases, CSF p-tau181 in patients with neuronal intranuclear inclusion disease (NIID) has not been studied.MethodsCSF concentrations of p-tau181, total tau, amyloid-beta 1-42 (Aβ42), monoamine metabolites homovanillic acid (HVA), and 5-hydroxyindole acetic acid (5-HIAA) were compared between 12 patients with NIID, 120 patients with symptomatic AD biologically confirmed based on CSF biomarker profiles, and patients clinically diagnosed with other neurocognitive disorders (dementia with Lewy bodies [DLB], 24; frontotemporal dementia [FTD], 13; progressive supranuclear palsy [PSP], 21; and corticobasal syndrome [CBS], 13). Amyloid PET using Pittsburgh compound B (PiB) was performed in six NIID patients.ResultsCSF p-tau181 concentration was significantly higher in NIID (72.7 ± 24.8 pg/mL) compared to DLB, PSP, and CBS and was comparable between NIID and AD. CSF p-tau181 was above the cutoff value (50.0 pg/mL) in 11 of 12 NIID patients (91.7%). Within these patients, only two patients showed decreased CSF Aβ42, and these patients showed negative or mild local accumulation in PiB PET, respectively. PiB PET scans were negative in the remaining 4 patients tested. CSF HVA and 5-HIAA concentrations were significantly higher in patients with NIID compared to disease controls.DiscussionCSF p-tau181 was increased in patients with NIID without amyloid accumulation. Although the deposition of p-tau has not been reported in NIID brains, molecular mechanism of tau phosphorylation or secretion of p-tau may be altered in NIID.

Background 18F-florbetapir is an amyloid β (Aβ) -targeted 18F-labeled positron emission tomography (PET) tracer for the clinical diagnosis of Alzheimer's disease. The standardized uptake value ratio (SUVR) serves as a tool with which to differentially diagnose. The present study aimed to cross-validate and compare SUVR derived from Amygo neuro and MIMneuro software. Methods We injected 40 individuals with 18F-florbetapir and then acquired PET images from 50 to 60 minutes later. All images were separately normalized to the standard 18F-florbetapir PET template using Amygo neuro and MIMneuro. Volumes of interest (VOIs) were automatically placed on six target regions each in Amygo neuro and MIMneuro. The composite SUVR (cSUVR) and regional SUVR (rSUVR) were calculated from mean values measured in VOI. A cSUVR of>1.10 was defined as representing Aβ positivity. Correlation coefficients were calculated in the two types of software. Results A cSUVR>1.10 was determined by Amygo neuro and MIMneuro in 15 of the 40 individuals. The rSUVR in the posterior cingulate, parietal lobe, precuneus, and temporal lobe significantly differed between Amygo neuro and MIMneuro, whereas the cSUVR did not. The SUVR calculated by the two types of software closely correlated to each other (R=0.89-0.96, P Conclusions The cSUVR was not different between Amygo neuro and MIMneuro. We suggest that Amygo neuro is comparable to MIMneuro in quantitative analysis using SUVR for 18F-florbetapir imaging, thus facilitating the use of standardized quantitative approaches to amyloid PET imaging.

Voxel-based morphometry (VBM) analysis of nuclear Magnetic Resonance Imaging (MRI) data allows the identification of medial temporal lobe (MTL) atrophy and is widely used to assist the diagnosis of Alzheimer’s disease (AD). However, its reliability in the clinical environment has not yet been confirmed. To determine the credibility of VBM, amyloid positron emission tomography (PET) and VBM studies were compared retrospectively. Patients who underwent Pittsburgh Compound B (PiB) PET were retrospectively recruited. Ninety-seven patients were found to be amyloid negative and 116 were amyloid positive. MTL atrophy in the PiB positive group, as quantified by thin sliced 3D MRI and VBM software, was significantly more severe (p =0.0039) than in the PiB negative group. However, data histogram showed a vast overlap between the two groups. The area under the ROC curve (AUC) was 0.646. MMSE scores of patients in the amyloid negative and positive groups were also significantly different (p = 0.0028), and the AUC was 0.672. Thus, MTL atrophy could not reliably differentiate between amyloid positive and negative patients in a clinical setting, possibly due to the wide array of dementia-type diseases that exist other than AD.

Background Alzheimer's disease (AD) and dementia with Lewy bodies (DLB) are often misdiagnosed with each other because of similar symptoms including progressive memory loss. The metabolic network topology that describes inter-regional metabolic connections can be generated using fluorodeoxyglucose positron emission tomography (FDG-PET) data with the graph-theoretical method. We hypothesized that different metabolic connectivity underlies the symptoms of AD patients, DLB patients, and cognitively normal (CN) individuals. Objective This study aimed to generate metabolic connectivity using FDG-PET data and assess the network topology to differentiate AD patients, DLB patients, and CN individuals. Methods This study included 45 AD patients, 18 DLB patients, and 142 CN controls. We analyzed FDG-PET data using the graph-theoretical method and generated the network topology in AD patients, DLB patients, and CN individuals. We statistically assessed the topology with global and nodal parameters. Results The whole metabolic network was preserved in CN; however, diffusely decreased connection was found in AD and partially but more deeply decreased connection was observed in DLB. The metabolic topology revealed that the right posterior cingulate and the left transverse temporal gyrus were significantly different between AD and DLB. Conclusion The present findings indicate that metabolic connectivity decreased in both AD and DLB, compared with CN. DLB was characterized restricted but deeper stereotyped network disruption compared with AD. The right posterior cingulate and the left transverse temporal gyrus are significant regions in the metabolic connectivity for differentiating AD from DLB.

Objective To evaluate the reproducibility of cerebral adenosine A(2A) receptor (A(2A)R) quantification using [C-11]preladenant ([C-11]PLN) and PET in a test-retest study.Methods Eight healthy male volunteers were enrolled. Dynamic 90 min PET scans were performed twice at the same time of the day to avoid the effect of diurnal variation. Subjects refrained from caffeine from 12 h prior to scanning, and serum caffeine was measured before radioligand injection. Arterial blood was sampled repeatedly during scanning and the fraction of the parent compound in plasma was determined. Total distribution volume (V-T) was estimated using 1- and 2-tissue compartment models (1-TCM and 2-TCM, respectively) and Logan graphical analysis (Logan plot) (t* = 30 min). Plasma-free fraction (f(P)) of [C-11]PLN was measured and used for correction of V-T values. Distribution volume ratio (DVR) was calculated from V-T of target and reference regions and obtained by noninvasive Logan graphical reference tissue model (LGAR) (t* = 30 min). Absolute test-retest variability (aTRV), and intra-class correlation coefficient (ICC) of V-T and DVR were calculated as indexes of repeatability. Correlation between DVR and serum concentration of caffeine (a nonselective A(2A)R blocker) was analyzed by Pearson's correlation analysis.Results Regional time-activity curves were well described by 2-TCM models. Estimation of V-T by 2-TCM produced some erroneous values; therefore, the more robust Logan plot was selected as the appropriate model. Global mean aTRV was 20% for V-T and 14% for V-T/f(P) (ICC, 0.72 for V-T and 0.87 for V-T/f(P)). Global mean aTRV of DVR was 13% for Logan plot and 10% for LGAR (ICC, 0.70 for Logan plot and 0.81 for LGAR). DVR estimates using LGAR and Logan plot were in good agreement (r(2) = 0.96). Coefficients of variation for V-T, V-T/f(P), DVR (Logan plot), and DVR (LGAR) were 47%, 47%, 27%, and 18%, respectively. Despite low serum caffeine levels, significant concentration-dependent effects on [C-11]PLN binding to target regions were observed (p < 0.01).Conclusions In this study, moderate test-retest reproducibility and large inter-subject differences were observed with [C-11]PLN PET, possibly attributable to competition by baseline amount of caffeine. Analysis of plasma caffeine concentration is recommended during [C-11]PLN PET studies.

Shortening the amount of time required to acquire amyloid positron emission tomography (PET) brain images while maintaining the accuracy of quantitative evaluation would help to overcome motion artifacts associated with Alzheimer's disease patients. The present study aimed to validate the quantitative accuracy of [

Coffee intake can decrease the risk for Parkinson's disease (PD). Its beneficial effects are allegedly mediated by caffeine through adenosine AWe aimed to calculate occupancy rates of striatal AFive patients with PD underwentThe mean serum caffeine level (μg/mL) was 0.374 at baseline and increased to 4.48 and 8.92 by 129.5 and 259 mg of caffeine, respectively. The mean occupancy rates of striatal AA sufficient A

Cerebral blood flow (CBF) / cerebral blood volume (CBV) ratio derived by [15O] H2O/ CO2 and CO positron emission tomography (PET) examination has been used as an index for cerebral perfusion pressure (CPP). CBF/CBV was demonstrated to be related mean arterial pressure (MAP) in baboons. However, this formula has not been confirmed to be proportionate to CPP. We have developed a new index for CPP using the Poiseuille equation based on a simple model. Our model suggests that CBF/CBV2 is proportionate to CPP and that it is mathematically a more accurate index than CBF/CBV. This new index needs experimental validation in the future.

To evaluate the reproducibility of cerebral adenosine AEight healthy male volunteers were enrolled. Dynamic 90 min PET scans were performed twice at the same time of the day to avoid the effect of diurnal variation. Subjects refrained from caffeine from 12 h prior to scanning, and serum caffeine was measured before radioligand injection. Arterial blood was sampled repeatedly during scanning and the fraction of the parent compound in plasma was determined. Total distribution volume (VRegional time-activity curves were well described by 2-TCM models. Estimation of VIn this study, moderate test-retest reproducibility and large inter-subject differences were observed with [UMIN000030040.

Two patients with different amyotrophic lateral sclerosis (ALS) phenotypes underwent 18F-THK5351 PET to visualize lesions undergoing astrogliosis by measuring monoamine oxidase B activity. Patient 1 was a 57-year-old man with flail leg syndrome. Elevated uptake was observed inside the motor cortex, corresponding to the leg area in a cortical homunculus. Patient 2 was a 64-year-old man with ALS-frontotemporal dementia semantic variant. Elevated uptake was observed around the left anterior temporal lobe. Both core lesions were consistent with their respective neurological features. Hence, 18F-THK5351 PET is a useful technique to assess ALS pathophysiology by visualizing the core lesions.

Three patients with neurological disorders (cerebral infarction, progressive multifocal leukoencephalopathy, and multiple sclerosis) underwent F-THK5351 and C-L-deprenyl PET on the same day to visualize lesions undergoing astrogliosis by measuring MAO-B activity. BPND map and SUV image with F-THK5351 as well as Ki map, Ki/K1 map and SUV image with C-L-deprenyl were created. F-THK5351 BPND maps and SUV images clearly identified the lesions undergoing astrogliosis. C-L-deprenyl Ki/K1 maps were close to F-THK5351 images, but very noisy. Ki maps and SUV images were likely affected by the effect of blood flow. Hence, F-THK5351 is superior to C-L-deprenyl for visualizing lesions undergoing astrogliosis.

We analyze the interaction of antineutrinos with water particle in electrochemical detectors. We postulate that some biological products generate a scalar auxiliary field B0 which breaks low-energy antineutrinos into boson vb and fermion v f particles. Low-energy anti neutrinos are suggested to interact with water molecules and produce output currents. We examine the output current of neutrino interactions in the electrochemical apparatus with chemical-reaction equations and half-cell model under postulated influence of weak interaction. The environmental neutrino is analysed. The output currents are treated to be generated by hydrogen ion and oxygen with the half-cell model with inclusion of weak interaction effect on hydrooxide ion recombination.

著者人数: 13名, Accepted: 2018-11-23, 資料番号: SA1180407000

Istradefylline, an adenosine A2A receptor (A2AR) antagonist, is effective as an adjunct to levodopa and can alleviate “off” time and motor symptoms in patients with Parkinson's disease (PD). The present study aimed to calculate occupancy rates of A2ARs by administrating istradefylline 20 mg or 40 mg, which is the currently approved dose for PD in Japan. Additionally, A2AR availability was compared between patients with PD and healthy controls. Ten patients with PD under levodopa therapy and six age-matched healthy controls were included. The patients underwent a total of two 11C-preladenant positron emission tomography scans before and after the administration of istradefylline 20 mg or 40 mg (both n = 5). Binding potential (BPND) was calculated to estimate A2AR availability in the ventral striatum, caudate, and putamen. Maximal A2AR occupancy and ED50 were estimated by modeling the dose-occupancy curves. All patients were around the middle stage of PD, and their characteristics were clinically heterogeneous. Maximal A2AR occupancy and ED50 were 93.5% and 28.6 mg in the ventral striatum, 69.5% and 10.8 mg in the caudate, and 66.8% and 14.8 mg in the putamen, respectively. There were no significant differences in BPND values in the ventral striatum (P = 0.42), caudate (P = 0.72), and putamen (P = 0.43) between the PD and control groups. In conclusion, the present study shows that istradefylline binds to A2ARs dose-dependently. A sufficient occupancy of A2ARs could be obtained by administrating the approved dose of istradefylline.

5-(1-(2-[[No serious adverse events occurred throughout the study period. Although biodistribution implied hepatobiliary excretion, secretion of radioactivity from liver to small intestine through the gallbladder was very slow. Total renal excreted radioactivity recovered during 6 h after injection was 2%ID. Absorbed dose was the highest in the pancreas (mean ± SD, 203 ± 45 μGy/MBq) followed by the liver (83 ± 11 μGy/MBq). Mean effective dose with and without urination was 17 ± 1 μSv/MBq. [This initial evaluation indicated that [

Little evidence exists on the role of type 1 metabotropic glutamate receptor (mGluR1) in the pathophysiology of Alzheimer's disease (AD), although mGluR1 may be involved in the regulation of neuronal excitability and synaptic plasticity. We have recently reported that mGluR1 availability in the early stage of AD is equivalent to that in healthy subjects. This study aimed to address whether mGluR1 availability changes with the progression of AD.Eight patients with AD (79.1 ± 4.6 years) underwent a total of two positron emission tomography (PET) examinations using the mGluR1 radioligand during the early-to-middle stages of AD. The mean interval was 2.8 years. Volumes-of-interest were placed on the frontal, parietal, and temporal cortices, hippocampus, anterior and posterior lobes, and vermis in the cerebellum. The binding potential (BPNo significant difference was observed in BPThis study suggests that mGluR1 availability is unchanged in the follow-up period of a few years during the early-to-middle stages of AD.

Background Silicon photomultiplier-positron emission tomography (SiPM-PET) has better sensitivity, spatial resolution, and timing resolution than photomultiplier tube (PMT)-PET. The present study aimed to clarify the advantages of SiPM-PET in 18F-fluoro-2-deoxy-D-glucose ([18F]FDG) brain imaging in a head-to-head comparison with PMT-PET in phantom and clinical studies. Methods Contrast was calculated from images acquired from a Hoffman 3D brain phantom, and image noise and uniformity were calculated from images acquired from a pool phantom using SiPM- and PMT-PET. Sequential PMT-PET and SiPM-PET [18F]FDG images were acquired over a period of 10 min from 22 controls and 10 patients. All images were separately normalized to a standard [18F]FDG PET template, then the mean standardized uptake values (SUVmean) and Z-score were calculated using MIMneuro and CortexID Suite, respectively. Results Image contrast, image noise, and uniformity in SiPM-PET changed 19.2, 3.5, and − 40.0% from PMT-PET, respectively. These physical indices of both PET scanners satisfied the criteria for acceptable image quality published by the Japanese Society of Nuclear Medicine of contrast > 55%, CV ≤ 15%, and SD ≤ 0.0249, respectively. Contrast was 70.0% for SiPM-PET without TOF and 59.5% for PMT-PET without TOF. The TOF improved contrast by 3.5% in SiPM-PET. The SUVmean using SiPM-PET was significantly higher than PMT-PET and did not correlate with a time delay. Z-scores were also significantly higher in images acquired from SiPM-PET (except for the bilateral posterior cingulate) than PMT-PET because the peak signal that was extracted by the calculation of Z-score in CortexID Suite was increased. The hypometabolic area in statistical maps was reduced and localized using SiPM-PET. The trend was independent of whether the images were derived from controls or patients. Conclusions The improved spatial resolution and sensitivity of SiPM-PET contributed to better image contrast and uniformity in brain [18F]FDG images. The SiPM-PET offers better quality and more accurate quantitation of brain PET images. The SUVmean and Z-scores were higher in SiPM-PET than PMT-PET due to improved PVE. [18F]FDG images acquired using SiPM-PET will help to improve diagnostic outcomes based on statistical image analysis because SiPM-PET would localize the distribution of glucose metabolism on Z-score maps.

We performed quartz crystal microbalance experiments using a 5-MHz AT-cut crystal for superfluid $^{4}\mathrm{He}$ films on exfoliated graphite (Grafoil) containing up to 0.40 atom/${\mathrm{nm}}^{2} ^{3}\mathrm{He}$. We found that the mass decoupling of $^{4}\mathrm{He}$ solid layers from the oscillating substrate is considerably sensitive, even with small amounts of $^{3}\mathrm{He}$. For a $^{4}\mathrm{He}$ film of 29.3 atoms/${\mathrm{nm}}^{2}$, we observed a small drop in resonant frequency at a ${T}_{3}$ of $\ensuremath{\sim}0.4$ K for a low oscillation amplitude, which is attributed to the sticking of $^{3}\mathrm{He}$ atoms at the $^{4}\mathrm{He}$ solid layer. For higher amplitudes, the $^{4}\mathrm{He}$ solid layer shows a reentrant mass decoupling at ${T}_{R}$ close to ${T}_{3}$. This decoupling can be explained by the suppression of the superfluid counterflow owing to the adsorption of the $^{3}\mathrm{He}$ atoms on edge dislocations. As the $^{4}\mathrm{He}$ areal density increases, ${T}_{R}$ shifts to a lower temperature and disappears around the $^{4}\mathrm{He}$ film of 39.0 atoms/${\mathrm{nm}}^{2}$.

Background Silicon photomultiplier-positron emission tomography (SiPM-PET) has better sensitivity, spatial resolution, and timing resolution than photomultiplier tubes (PMT)-PET. The present study aimed to clarify the advantages of SiPM-PET in 18F-fluoro-2-deoxy-D-glucose ([18F]FDG) brain imaging in a head-to-head comparison with PMT-PET in phantom and clinical studies. Methods Image contrast was calculated from images acquired from a Hoffman 3D brain phantom and image noise and uniformity were calculated from pooled images acquired from a pool phantom using SiPM- and PMT-PET. Sequential PMT-PET and SiPM-PET [18F]FDG images were acquired over a period of 10 min from 22 individuals. All images were separately normalized to a standard [18F]FDG PET template, then mean standardized uptake values (SUVmean) and Z-score were calculated by MIMneuro and Cortex ID Suite, respectively. Results Image contrast, image noise, and uniformity in SiPM-PET changed 27.5%, -2.1%, and − 138.2% from PMT-PET, respectively. These physical indices of SiPM-PET satisfied the criteria for acceptable image quality published by the Japanese Society of Nuclear Medicine of > 55%, ≤ 15% and ≤ 0.0249, respectively. The residual background count was reduced with time-of-flight algorithm especially in SiPM-PET. The SUVmean using SiPM-PET was significantly higher than PMT-PET and did not correlate with a time delay. Z-scores were also significantly higher in images acquired from SiPM-PET (except for the bilateral posterior cingulate) than PMT-PET because the peak signal that was extracted by the calculation of Z-score in Cortex ID Suite was raised. Conclusions The better spatial and timing resolution, and sensitivity in SiPM-PET were contributed to better image contrast, image noise, and uniformity on brain [18F]FDG images. SiPM-PET offers better quality and more accurate quantitation of brain PET images. The SUVmean and Z-score in SiPM-PET was higher than PMT-PET. [18F]FDG images acquired using SiPM-PET will help to improve diagnostic outcomes based on the statistical image analysis because the SiPM-PET was more localized the distribution of glucose metabolism on Z-score maps.

Background Silicon photomultiplier-positron emission tomography (SiPM-PET) has better sensitivity, spatial resolution, and timing resolution than photomultiplier tube (PMT)-PET. The present study aimed to clarify the advantages of SiPM-PET in 18F-fluoro-2-deoxy-D-glucose ([18F]FDG) brain imaging in a head-to-head comparison with PMT-PET in phantom and clinical studies. Methods Contrast was calculated from images acquired from a Hoffman 3D brain phantom, and image noise and uniformity were calculated from images acquired from a pool phantom using SiPM- and PMT-PET. Sequential PMT-PET and SiPM-PET [18F]FDG images were acquired over a period of 10 min from 22 controls and 10 patients. All images were separately normalized to a standard [18F]FDG PET template, then the mean standardized uptake values (SUVmean) and Z-score were calculated using MIMneuro and CortexID Suite, respectively. Results Image contrast, image noise, and uniformity in SiPM-PET changed 19.2, 3.5, and − 40.0% from PMT-PET, respectively. These physical indices of both PET scanners satisfied the criteria for acceptable image quality published by the Japanese Society of Nuclear Medicine of contrast > 55%, CV ≤ 15%, and SD ≤ 0.0249, respectively. Contrast was 70.0% for SiPM-PET without TOF and 59.5% for PMT-PET without TOF. The TOF improved contrast by 3.5% in SiPM-PET. The SUVmean using SiPM-PET was significantly higher than PMT-PET and did not correlate with a time delay. Z-scores were also significantly higher in images acquired from SiPM-PET (except for the bilateral posterior cingulate) than PMT-PET because the peak signal that was extracted by the calculation of Z-score in CortexID Suite was increased. The hypometabolic area in statistical maps was reduced and localized using SiPM-PET. The trend was independent of whether the images were derived from controls or patients. Conclusions The improved spatial resolution and sensitivity of SiPM-PET contributed to better image contrast and uniformity in brain [18F]FDG images. The SiPM-PET offers better quality and more accurate quantitation of brain PET images. The SUVmean and Z-scores were higher in SiPM-PET than PMT-PET due to improved PVE. [18F]FDG images acquired using SiPM-PET will help to improve diagnostic outcomes based on statistical image analysis because SiPM-PET would localize the distribution of glucose metabolism on Z-score maps. Supplementary Information The online version contains supplementary material available at 10.1186/s40658-020-00337-4.

Background Brain F-FDG uptake reportedly starts to decline more than 10 years before the onset of cognitive decline in dominantly inherited Alzheimer disease (AD). We compared longitudinal F-FDG images in sporadic AD to aging data from a large sample size to expand the current knowledge of F-FDG reduction for AD progression. Methods Participants comprised 2 individuals (subjects A and B at ages 65 and 68 years, respectively) and 107 control subjects (67.9 [SD, 4.9] years). Subject A underwent F-FDG PET a total of 8 times over 9 years from the preclinical to early dementia stages. Subject B underwent F-FDG PET a total of 11 times over 12 years from the preclinical to mild cognitive impairment stages. Control subjects underwent F-FDG PET twice over a mean follow-up period of 7.8 years. After placing the volume of interest on the AD-related hypometabolic regions, the longitudinal F-FDG images were compared among the subjects and control subjects. Results For the control group, the rate of F-FDG reduction was 2.2% per decade (ie, aging effects). The rates of F-FDG reduction were 9.41% over 9 years and 9.07% over 12 years in subjects A and B, respectively. We estimated that F-FDG uptake started to decrease 4 and 2 years before indications of memory loss in subjects A and B, respectively. Conclusions The present study suggests that the time between the beginning of F-FDG reduction and the onset of cognitive decline may be shorter in elderly individuals with AD compared with the recently estimated period in dominantly inherited AD.

Dynamic exercise elicits fluctuations in blood pressure (BP) and cerebral blood flow (CBF). This study investigated responses in BP and CBF during cycling exercise and post-exercise hypotension (PEH) using positron emission tomography (PET). CBF was measured using oxygen-15-labeled water (H2 15O) and PET in 11 human subjects at rest (Rest), at the onset of exercise (Ex1), later in the exercise (Ex2), and during PEH. Global CBF significantly increased by 13% at Ex1 compared with Rest, but was unchanged at Ex2 and during PEH. Compared with at Rest, regional CBF (rCBF) increased at Ex1 (20~42%) in the cerebellar vermis, sensorimotor cortex for the bilateral legs (M1Leg and S1Leg), insular cortex and brain stem, but increased at Ex2 (28~31%) only in the vermis and M1Leg and S1Leg. During PEH, rCBF decreased compared with Rest (8~13%) in the cerebellum, temporal gyrus, piriform lobe, thalamus and pons. The areas showing correlations between rCBF and mean BP during exercise and PEH were consistent with the central autonomic network, including the brain stem, cerebellum, and hypothalamus (R2=0.25–0.64). The present study suggests that higher brain regions are coordinated through reflex centers in the brain stem in order to regulate the cardiovascular response to exercise.

A 26-year-old woman with relapsing-remitting multiple sclerosis (MS) underwent F-THK5351 PET during a remission period. PET imaging showed that small regions with elevated uptake of F-THK5351 were scattered in the brain and that the foci of F-THK5351 accumulations corresponded anatomically to MS plaques identified by MRI. Because F-THK5351 binds to monoamine oxidase B highly expressed in astrocytes, F-THK5351 accumulates in lesions undergoing astrogliosis. Hence, elevated uptake of F-THK5351 in the present case can represent ongoing astrogliosis in inactive MS lesions (plaques).