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The role of torso computed tomography (CT) in evaluating body composition has been unexplored. This study assessed the potential of low-dose torso CT from positron emission tomography (PET)/CT for analyzing body composition and its relation to muscle strength. We retrospectively recruited 384 healthy Korean adults (231 men, 153 women) who underwent torso 18F-FDG PET/CT, bioelectrical impedance analysis (BIA), and muscle strength tests (handgrip strength [HGS] and knee extension strength [KES]). CT images were segmented into three compartments: torso volumetric, abdominal volumetric, and abdominal areal. Muscle amounts from each compartment were indexed to height (m2). BIA and HGS served as reference standards, with correlation coefficients (r) calculated. Torso muscle volumetric index (TorsoMVI) had the strongest correlations with BIA-derived values (r = 0.80 for men; r = 0.73 for women), surpassing those from the abdominal compartments. TorsoMVI was also correlated significantly with HGS (r = 0.39, p < 0.01) and differentiated between normal and possible sarcopenia in men (n = 225, 5960 ± 785 cm3/m2 vs. n = 6, 5210 ± 487 cm3/m2, p = 0.02). In women, KES correlated more strongly with muscle parameters than HGS. Despite gender-specific variations, torso CT-derived parameters show promise for evaluating body composition and sarcopenia. [ABSTRACT FROM AUTHOR]

We present the case of a 70-year-old male patient who underwent a gallium-68 (68Ga)-DOTATOC brain positron emission tomography (PET)/computed tomography (CT) for the assessment of a tumorous lesion on the dura. The patient had previously undergone below-knee amputation due to a mass of synovial sarcoma on the left foot and completed adjuvant chemotherapy approximately 3 months ago. Subsequently, a well-demarcated papillary solid mass located on the dura was surgically excised. Pathological examination confirmed that the dural metastasis originated from synovial sarcoma and post-operative magnetic resonance imaging (MRI) revealed no residual tumor. We conducted a 68Ga-DOTATOC brain PET/CT suspecting a meningioma given the presence of a dural mass. The result showed lower uptake (maximum standardized uptake [SUVmax 4.9]) than the pituitary gland (SUVmax 9.3). Thus, we successfully conducted a differential diagnosis of metastasis from the preexisting malignancy rather than the meningioma. 68Ga-DOTATOC PET/CT is a valuable tool for the differential diagnosis of meningioma. However, metastasis should also be considered, especially in patients with a history of malignancy and lesions showing mild 68Ga-DOTATOC uptake. [ABSTRACT FROM AUTHOR]

Purpose: This study aimed to compare the clinical significance of two parameters, division of standardized uptake value (SUV) of target arterial activity by background venous blood pool activity (SUVA/V) and subtraction of background venous blood pool activity from SUV of target arterial activity (SUVA-V) of carotid arteries with atherosclerotic plaques using 18F-fluorodeoxyglucose (FDG) positron emission tomography and computed tomography (PET/CT). Methods: Patients aged 50 years or more who were diagnosed with carotid artery stenosis of 50% or more with carotid Doppler ultrasonography and had torso 18F-FDG PET/CT were enrolled retrospectively and classified patients who developed cerebrovascular events (CVEs) within 5 years after 18F-FDG PET/CT scan as the active group and patients who did not experience the CVE within 5 years as an inactive group. We calculated SUVA/V and SUVA-V using measurements of SUVmax of carotid arteries and mean SUV of superior vena cava (SVC). Results: SUVA-V, SUVA-V_high, and SUVA-V_low were significantly higher in the active group than in the inactive group, but neither SUVA/V, SUVA/V_high, nor SUVA/V_low showed significant differences between the active and inactive groups. The difference in rank between groups of SUVA/V_high and SUVA/V_low was greater than the difference in rank between groups of SUVA-V_high and SUVA-V_low. The CVE incidence differed between SUVA/V_high and SUVA/V_low of high carotid FDG uptake, but the CVE incidence did not differ between SUVA-V_high and SUVA-V_low of high carotid FDG uptake. Conclusion: SUVA-V may be a more rational solution than SUVA/V for evaluating atherosclerotic plaque inflammation on 18F-FDG PET/CT. [ABSTRACT FROM AUTHOR]

18F-FP-CIT is a high-resolution imaging marker of nigrostriatal neuronal integrity, differentiating Parkinsonism with loss of dopaminergic terminals (presynaptic Parkinsonian syndrome [PS]) from Parkinsonism without nigrostriatal degeneration (non-PS). We assessed the diagnostic accuracy of 18F-FP-CIT PET in patients with clinically uncertain PS (CUPS) at the first visit. Among the 272 patients who underwent 18F-FP-CIT PET imaging at the first visit between September 2008 and July 2012, 111 had CUPS (age, 62.6 ± 10.5 y; male:female, 45:66; symptom duration, 13.1 ± 8.8 months). Uncertainty criteria included only one of the three cardinal signs of Parkinsonism, two signs without bradykinesia, or atypical signs. The baseline clinical and 18F-FP-CIT PET imaging diagnostic accuracy was compared with the accuracy of clinical diagnosis after > 2-year follow-up. Nuclear medicine physicians assessed the 18F-FP-CIT PET images visually. Focal dopamine transporter binding deficit in the posterior putamen was considered PS. Bilateral symmetric striatum without focal deficit, suggesting normal 18F-FP-CIT PET, and focal deficits elsewhere in the striatum suggesting vascular Parkinsonism were considered non-PS. Seventy-nine patients had PS, and 32 did not. Baseline clinical diagnosis included PS in 45 patients, non-PS in 24, and inconclusive in 42. Among patients in whom initial clinical diagnosis (PS or non-PS) was possible, the sensitivity, specificity, and accuracy of the baseline clinical and 18F-FP-CIT PET imaging diagnoses were 54.4, 50.0, and 53.2%, and 98.7, 100, and 99.1%, respectively. The respective positive and negative predictive values were 95.6 and 66.7%, and 100 and 97.0%. Among those with initially inconclusive diagnosis, 64.2% were eventually diagnosed with PS while 35.7% were diagnosed with non-PS. The final clinical diagnosis of these patients all matched those made by 18F-FP-CIT PET imaging, except in one patient with scan without evidence of dopaminergic deficit (SWEDD). 18F-FP-CIT PET diagnosis was more accurate than clinical diagnosis, reducing the false-negative and inconclusive clinical diagnosis rates at baseline in patients with CUPS. [ABSTRACT FROM AUTHOR]

We developed a novel quantification method named "shape feature" by combining the features of amyloid positron emission tomography (PET) and brain magnetic resonance imaging (MRI) and evaluated its significance in predicting the conversion from mild cognitive impairment (MCI) to Alzheimer's disease (AD) in the Alzheimer's Disease Neuroimaging Initiative (ADNI) cohort. From the ADNI database, 334 patients with MCI were included. The brain amyloid smoothing score (AV45_BASS) and brain atrophy index (MR_BAI) were calculated using the surface area and volume of the region of interest in AV45 PET and MRI. During the 48-month follow-up period, 108 (32.3%) patients converted from MCI to AD. Age, Mini-Mental State Examination (MMSE), cognitive subscale of the Alzheimer's Disease Assessment Scale (ADAS-cog), apolipoprotein E (APOE), standardized uptake value ratio (SUVR), AV45_BASS, MR_BAI, and shape feature were significantly different between converters and non-converters. Univariate analysis showed that age, MMSE, ADAS-cog, APOE, SUVR, AV45_BASS, MR_BAI, and shape feature were correlated with the conversion to AD. In multivariate analyses, high shape feature, SUVR, and ADAS-cog values were associated with an increased risk of conversion to AD. In patients with MCI in the ADNI cohort, our quantification method was the strongest prognostic factor for predicting their conversion to AD. [ABSTRACT FROM AUTHOR]

We aimed to examine the associations of cardiovascular risk factors with myocardial perfusion reserve (MPR) in patients with type 2 diabetes and stable coronary artery disease. The study patients were retrospectively identified from a database of patients with diabetes and stable coronary artery disease at Asan Medical Center (Seoul, Republic of Korea), covering the period from 2017 to 2019. The primary outcome variable was MPR assessed by dynamic stress 201Tl/rest 99mTc-tetrofosmin SPECT. Univariable and stepwise multivariable analyses were performed to assess the associations of cardiovascular risk factors with MPR. A total of 276 patients (236 men and 40 women) were included. The median global MPR was 2.4 (interquartile range 1.9–3.0). Seventy-five (27.2%) patients had an MPR < 2.0. Multivariable linear regression showed that smoking (ß = − 0.44, 95% confidence interval − 0.68 to − 0.21, P < 0.001), hypertension (ß = − 0.24, 95% confidence interval − 0.47 to − 0.02, P = 0.033), and summed difference score (ß = − 0.05, 95% confidence interval − 0.07 to − 0.03, P < 0.001) were independently associated with MPR. Abnormal MPR (< 2.0) was associated with a higher incidence of cardiac death or myocardial infarction (P = 0.034). MPR assessed by dynamic stress 201Tl/rest 99mTc-tetrofosmin SPECT was impaired in a large cohort of patients with diabetes. After adjusting for risk variables, including standard myocardial perfusion imaging characteristics, smoking, and hypertension were associated with MPR. Our results may aid in identifying patients with impaired MPR and stratifying patients with type 2 diabetes. [ABSTRACT FROM AUTHOR]

Parkinson's disease (PD) is one of the most common neurodegenerative diseases caused by the loss of dopaminergic neurons in the substantia nigra pars compacta. Although the etiology of PD is still unclear, the death of dopaminergic neurons during PD progression was revealed to be associated with abnormal aggregation of α-synuclein, elevation of oxidative stress, dysfunction of mitochondrial functions, and increased neuroinflammation. In this study, the effects of Licochalcone D (LCD) on MG132-induced neurotoxicity in primitive neural stem cells (pNSCs) derived from reprogrammed iPSCs were investigated. A cell viability assay showed that LCD had anti-apoptotic properties in MG132-induced oxidative-stressed pNSCs. It was confirmed that apoptosis was reduced in pNSCs treated with LCD through 7-AAD/Annexin Ⅴ staining and cleaved caspase3. These effects of LCD were mediated through an interaction with JunD and through the EGFR/AKT and JNK signaling pathways. These findings suggest that LCD could be a potential antioxidant reagent for preventing disease-related pathological phenotypes of PD. [ABSTRACT FROM AUTHOR]

Background: Cerebral amyloid angiopathy (CAA) often presents as cognitive impairment, but the mechanism of cognitive decline is unclear. Recent studies showed that number of microbleeds were associated with cognitive decline.Objective: We aimed to investigate how microbleeds contribute to cognitive impairment in association with white matter tract abnormalities or cortical thickness in CAA.Methods: This retrospective comparative study involved patients with probable CAA according to the Boston criteria (Aβ+ CAA) and patients with Alzheimer's disease (Aβ+ AD), all of whom showed severe amyloid deposition on amyloid PET. Using mediation analysis, we investigated how FA or cortical thickness mediates the correlation between the number of lobar microbleeds and cognition.Results: We analyzed 30 patients with Aβ+ CAA (age 72.2±7.6, female 53.3%) and 30 patients with Aβ+ AD (age 71.5±7.6, female 53.3%). The two groups showed similar degrees of cortical amyloid deposition in AD-related regions. The Aβ+ CAA group had significantly lower FA values in the clusters of the posterior area than did the Aβ+ AD group(family-wise error-corrected p < 0.05). The correlation between the number of lobar microbleeds and visuospatial function was indirectly mediated by white matter tract abnormality of right posterior thalamic radiation (PTR) and tapetum, while lobar microbleeds and language function was indirectly mediated by the abnormality of left PTR and sagittal stratum. Cortical thickness did not mediate the association between lobar microbleeds and cognition.Conclusion: This result supports the hypothesis that microbleeds burden leads to white matter tract damage and subsequent cognitive decline in CAA. [ABSTRACT FROM AUTHOR]

The concept of cognitive reserve (CR) has been proposed as a protective factor that modifies the effect of brain pathology on cognitive performance. It has been characterized through CR proxies; however, they have intrinsic limitations. In this study, we utilized two different datasets containing tau, amyloid PET, and T1 magnetic resonance imaging. First, 91 Alzheimer's disease (AD) continuum subjects were included from Alzheimer's Disease Neuroimaging Initiative 3. CR was conceptualized as the residual between actual cognition and estimated cognition based on amyloid, tau, and neurodegeneration. The proposed marker was tested by the correlation with CR proxy and modulation of brain pathology effects on cognitive function. Second, longitudinal data of baseline 53 AD spectrum and 34 cognitively unimpaired (CU) participants in the MEMORI dataset were analyzed. CR marker was evaluated for the association with disease conversion rate and clinical progression. Applying our multimodal CR model, this study demonstrates the differential effect of CR on clinical progression according to the disease status and the modulating effect on the relationship between brain pathology and cognition. The proposed marker was associated with years of education and modulated the effect of pathological burden on cognitive performance in the AD spectrum. Longitudinally, higher CR marker was associated with lower disease conversion rate among prodromal AD and CU individuals. Higher CR marker was related to exacerbated cognitive decline in the AD spectrum; however, it was associated with a mitigated decline in CU individuals. These results provide evidence that CR may affect the clinical progression differentially depending on the disease status. [ABSTRACT FROM AUTHOR]

Amyloid (Aβ) and tau proteins are pathologic hallmarks of Alzheimer disease (AD). It is well known that there is spatial disparity between Aβ and tau protein deposition but, crossed hemispheric accumulation of these 2 proteins has not been reported. Here we report the case of a 76-year-old woman with typical AD who underwent amyloid positron emission tomography (PET) ([ 18 F]-florbetaben) and tau PET scans ([ 18 F]PI-2620), revealing crossed accumulation of Aβ and tau in the cerebral hemisphere. A neuropsychological assessment showed impairment in memory with spared activities of daily living. In the PET analysis, amyloid deposition was observed only in the left side of the cerebral hemisphere and tau only in the right side. Neuroimaging follow-up indicated that the spatial pattern of these protein accumulations had not changed. This case suggests the possibility of independent Aβ and tau pathogenic pathways in AD. [ABSTRACT FROM AUTHOR]

Background: To date, the clinical significance of visually equivocal amyloid positron emission tomography (PET) has not been well established. Objective: We studied the clinical significance of equivocal amyloid PET images from the Alzheimer's Disease Neuroimaging Initiative (ADNI). Methods: Subjects with F-18 florbetapir PET scans at baseline who were followed up for 4 years were selected. Clinical characteristics, imaging biomarkers, cognitive function, and rate of conversion to AD were compared in subjects with visually equivocal findings. Results: Of 249 subjects who completed the follow-up, 153 (61.4%), 20 (8.0%), and 129 (30.5%) were F-18 florbetapir-negative, -equivocal, and -positive, respectively. The mean standardized uptake value ratios (SUVR) of F-18 florbetapir PET were 0.75 ± 0.04, 0.85 ± 0.10, and 1.00 ± 0.09 for each group (p <0.001 between groups), and 15.0%, 70.0%, and 98.7% of patients were quantitatively above the positive threshold. The change in the SUVR of F-18 florbetapir PET was higher in the equivocal (6.09 ± 3.61%, p <0.001) and positive (3.13 ± 4.38%, p <0.001) groups than the negative group (0.88 ± 4.28%). Among the subjects with normal or subjective memory impairment and mild cognitive impairment, 5.3% with negative amyloid PET and 37.5% with positive amyloid PET converted to AD over the 4-year period. None of the equivocal amyloid PET subjects converted to AD during this period. Conclusion: Approximately 8% of subjects from the ADNI cohort showed visually equivocal amyloid PET scans with intermediate load and rapid accumulation of amyloid, but did not convert to AD during the 4-year follow-up. [ABSTRACT FROM AUTHOR]

Purpose: To assess the in vivo whole-brain relationship between uptake of [18F]THK-5351 on PET and cortical atrophy on structural MRI according to the presence and severity of Alzheimer's disease (AD). Materials and methods: Sixty-five participants (21 normal controls, 32 mild cognitive impairment [MCI] subjects, and 12 AD patients) were enrolled from a prospective multicenter clinical trial (NCT02656498). Structural MRI and [18F]THK-5351 PET were performed within a 2-month interval. Cortical volume and standardized uptake value ratios (SUVR) were calculated from MRI and PET images, respectively, for 35 FreeSurfer-derived cortical regions. Pearson's correlation coefficients between SUVR and cortical volume were calculated for the same regions, and correlated regions were compared according to disease severity and β-amyloid PET positivity. Results: No significantly correlated regions were found in the normal controls. Negative correlations between SUVR and cortical volume were found in the MCI and AD groups, mainly in limbic locations in MCI and isocortical locations in AD. The AD group exhibited stronger correlations (r = −0.576–0.781) than the MCI group (r = 0.368–0.571). Hippocampal atrophy did not show any correlation with SUVR in the β-amyloid PET-negative group, but negatively correlated with SUVR (r = −0.494, P =.012) in the β-amyloid PET-positive group. Conclusions: Regional THK-5351 uptake correlated more strongly with cortical atrophy in AD compared with MCI, thereby demonstrating a close relationship between the neuro-pathologic process and cortical atrophy. Hippocampal atrophy was associated with both β-amyloid and THK-5351 uptake, possibly reflecting an interaction between β-amyloid and tau deposition in the neurodegeneration process. [ABSTRACT FROM AUTHOR]

Keywords: draft genome; hybrid assembly; Liza haematocheila; ortholog and phylogenetic analysis; repeat analysis According to the k-mer size estimations, similar genome lengths (698-714 Mb) were observed, and the estimated genome size of I L. haematocheila i was 700 Mb. Therefore, the hybrid assembly approach used in this study was considered effective in reducing the number of contigs and increasing the contig N50 length of the heterozygous diploid genome, by combining Illumina HiSeq short-read and PacBio long-read sequences. Draft genome, hybrid assembly, Liza haematocheila, ortholog and phylogenetic analysis, repeat analysis. [Extracted from the article]

Background: We investigated longitudinal changes in cortical tau accumulation and their association with cognitive decline in patients with Alzheimer's disease (AD) spectrum using [18F]PI‐2620 PET. Method: We enrolled 54 (69.9±8.5 y, M:F = 16:38) participants (8 cognitively normal [NC], 28 mild cognitive impairment [MCI], 18 AD) who completed [18F]PI‐2620 PET scans at baseline and 1 y follow up. Subject also underwent [18F]florbetaben PET (baseline only), MRI and neuropsychological tests. Aβ PET images were visually scored as positive or negative. Aβ+ MCI & AD were classified into early onset (<65 y, EO+) and late onset (≥65, LO+) group. Standardized uptake value ratios (SUVr) of [18F]PI‐2620 PET were determined by cerebral to inferior cerebellar ratio and corrected for partial volume effect. Cortical volumes were calculated from 3D T1‐weighted MR images. We also investigated a correlation between the progression of tau accumulation and cognitive decline. Result: Thirty eight out of 57 participants showed Aβ+ (1 NC, 20 MCI, 17 AD). Global SUVr values of [18F]PI‐2620 PET were 0.96±0.07 in 7 Aβ‐ NC, 1.23±0.41 in 17 LO+ (76.7±3.8y) and 1.86±0.87 in 20 EO+ (63.4±5.4y) (p<0.001). It increased by 0.09±0.14 (7.0%) in LO+ and 0.14±0.27 (11.6%) in EO+ in contrast to no change in NC‐. EO+ showed abundant tau accumulation in Braak III‐V areas at baseline with rapid accumulation in Braak V area (0.33±0.41 [13.9%] vs. 0.08±0.14 [6.7%], p = 0.010) than LO+ group. It showed abundant and rapid accumulation on Braak 3 areas in LO+ group (1.61±0.53 at baseline, change: 0.15±0.25 [8.2%]). Deterioration of the visuospatial function and verbal memory was associated with the progression of tau accumulation in Braak III‐V areas in EO+ group. Progressive atrophy in Braak III‐V areas were associated with the progression of tau accumulation in LO+ group whereas hippocampal atrophy did in EO+ group. Conclusion: Tau accumulation measured by [18F]PI‐2620 in EO+ showed rapid accumulation in Braak III‐V areas and correlated with deterioration of the visuospatial function and verbal memory. It suggests that [18F]PI‐2620 PET is potential biomarker for selecting therapeutic target and monitoring treatment effect for tau targeting treatment. [ABSTRACT FROM AUTHOR]

Purpose: We investigated the regional distribution of 18F-THK5351 uptake in gray (GM) and white matter (WM) in patients with behavioral-variant frontotemporal dementia (bvFTD) and compared it with that in patients with Alzheimer's disease (AD) or semantic dementia (SD).Methods: 18F-THK-5351 positron emission tomography (PET), 18F-florbetaben PET, magnetic resonance imaging, and neuropsychological testing were performed in 103 subjects including 30, 24, 9, and 8 patients with mild cognitive impairment, AD, bvFTD, and SD, respectively, and 32 normal subjects. Standardized uptake value ratios (SUVRs) of 18F-THK-5351 PET images were measured from six GM and WM regions using cerebellar GM as reference. GM and WM SUVRs and WM/GM ratios, the relationship between GM SUVR and WM/GM ratio, and correlation between SUVR and cognitive function were compared.Results: In AD, both parietal GM (p < 0.001) and WM (p < 0.001) SUVRs were higher than in bvFTD. In AD and SD, the WM/GM ratio decreased as the GM SUVR increased, regardless of lobar region. In AD, memory function correlated with parietal GM (ρ = −0.74, p < 0.001) and WM (ρ = −0.53, p < 0.001) SUVR. In SD, language function correlated with temporal GM SUVR (ρ = −0.69, p = 0.006). The frontal WM SUVR was higher in bvFTD than in AD (p = 0.003) or SD (p = 0.017). The frontal WM/GM ratio was higher in bvFTD than in AD (p < 0.001). In bvFTD, the WM/GM ratio increased more prominently than the GM SUVR only in the frontal lobe (R2 = 0.026). In bvFTD, executive function correlated with frontal WM SUVR (ρ = −0.64, p = 0.014).Conclusions: Frontal WM 18F-THK5351 uptake was higher in bvFTD than in other dementias. The increase in frontal WM uptake was greater than the increase in GM uptake and correlated with executive function. This suggests that frontal lobe WM 18F-THK5351 uptake reflects neuropathological differences between bvFTD and other dementias. [ABSTRACT FROM AUTHOR]