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Background Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that impairs both upper and lower motor neurons. Mutations in the neurofilament heavy (NEFH) gene are associated with a higher risk for ALS. This study aimed to evaluate the brain metabolism in patients with ALS and NEFH gene mutations (NEFH‐ALS) and assess its correlation with emotional and cognitive changes. Methods This prospective study enrolled 119 patients with ALS and 128 age‐ and gender‐matched health controls. Study assessments included demographic data collection, questionnaires for motor function, cognition, and depression, and brain F‐18 FDG PET/CT (18F‐fluorodeoxyglucose positron emission tomography (PET)/computed tomography (CT)) scan. Correlation between brain metabolism and clinical questionnaire scores was performed. Chain‐mediation model analysis for the NEFH‐ALS group was conducted. Cox regression and Kaplan–Meier survival analysis were also performed. Results There were 26 NEFH‐ALS patients. Patients with NEFH‐ALS showed brain glucose hypometabolism in the cortex‐striatum/limbic system‐brainstem circuit when compared with healthy controls (p < 0.05). Decreased brain glucose metabolism was correlated with impairments of motor function (r = 0.477, p = 0.014, FDR corrected p = 0.014), cognitive scores (r = 0.549, p = 0.004, FDR corrected p = 0.009), and depression (r = −0.523, p = 0.009, FDR corrected p = 0.009). This study showed that brain glucose hypometabolism could lead to impairment of motor function, which was mediated by cognition and depression. Survival analysis showed that brain glucose metabolism was an independent prognostic factor for patients with ALS. Conclusions Reduced brain glucose metabolism in the cortex‐striatum/limbic system‐brainstem circuit may potentially serve as an independent prognostic factor for patients with ALS and NEFH mutation. NEFH‐ALS had brain glucose hypometabolism of the cortex‐striatum/limbic system‐brainstem circuit, correlated with motor function, cognition, and depression. Brain glucose hypometabolism could lead to impairment of motor function, which was mediated by cognition and depression. The reduced brain metabolism could potentially be an independent prognostic factor for survival.

Purpose Positron emission tomography (PET) with the first and only tau targeting radiotracer of 18 F-flortaucipir approved by FDA has been increasingly used in depicting tau pathology deposition and distribution in patients with cognitive impairment. The goal of this international consensus is to help nuclear medicine practitioners procedurally perform 18 F-flortaucipir PET imaging. Method A multidisciplinary task group formed by experts from various countries discussed and approved the consensus for 18 F-flortaucipir PET imaging in Alzheimer’s disease (AD), focusing on clinical scenarios, patient preparation, and administered activities, as well as image acquisition, processing, interpretation, and reporting. Conclusion This international consensus and practice guideline will help to promote the standardized use of 18 F-flortaucipir PET in patients with AD. It will become an international standard for this purpose in clinical practice.

We investigated the relationship of plasma amyloid beta (Aβ) with cerebral deposition of Aβ and tau on positron emission tomography (PET). Forty-four participants (18 cognitively normal older adults [CN], 10 mild cognitive impairment, 16 Alzheimer's disease [AD]) underwent amyloid PET and a blood draw. Free and total plasma Aβ40 and Aβ42 were assessed using a validated assay. Thirty-seven participants (17 CN, 8 mild cognitive impairment, 12 AD) also underwent a [18F]flortaucipir scan. Scans were preprocessed by standard techniques, and mean global and regional amyloid and tau values were extracted. Free Aβ42/Aβ40 (Aβ F42:F40) and total Aβ42/Aβ40 (Aβ T42:T40) were evaluated for differences by diagnosis and relation to PET Aβ positivity. Relationships between these measures and cerebral Aβ and tau on both regional and voxel-wise basis were also evaluated. Lower Aβ T42:T40 was associated with diagnosis and PET Aβ positivity. Lower plasma Aβ T42:T40 ratios predicted cerebral Aβ positivity, both across the full sample and in CN only. Finally, lower plasma Aβ T42:T40 ratios were associated with increased cortical Aβ and tau in AD-related regions on both regional and voxel-wise analyses. Plasma Aβ measures may be useful biomarkers for predicting cerebral Aβ and tau. Additional studies in larger samples are warranted.

INTRODUCTION Understanding neuroinflammation across the Alzheimer's disease (AD) spectrum is essential to elucidate disease mechanisms and individualize therapy. METHODS Human microglial translocator protein (TSPO) expression under inflammatory stimuli was assessed by immunoblot experiments. Ninety‐six participants were enrolled across four groups: cognitively unimpaired amyloid (CU A) + and −, mild cognitive impaired (MCI) A+, and Alzheimer's disease dementia (ADD) A+. Neuroinflammation using 11C‐ER176 TSPO positron emission tomography (PET) was compared to amyloid and tau PET. Correlations between neuroinflammation, amyloid, and tau pathology were examined across disease stages. RESULTS TSPO was upregulated in human microglia under AD‐like inflammatory conditions. Neuroinflammation, defined by PET TSPO, increased in CU A+ participants and became more widespread with increasing disease severity, aligning with worsening amyloid and tau pathology. Associations with tau were particularly extensive in temporal and parietal regions. DISCUSSION These findings suggest probable amyloid association with early microglial activation, while tau pathology is closely tied to wider distribution of neuroinflammation. Highlights TSPO expression increases in human microglia under AD‐like inflammation. 11C‐ER176 PET shows stage‐dependent neuroinflammation across the AD spectrum. Neuroinflammation overlaps with tau and is more widespread in amyloid‐positive individuals. Activity peaks in MCI, stabilizes later, and relates to vascular and neurodegenerative changes.

Background Reduced 18 F-fluorodeoxyglucose-positron emission tomography (FDG-PET) brain metabolism was recognized as a biomarker of neurodegeneration in the recently proposed ATN framework for Alzheimer’s disease (AD) biological definition. However, accumulating evidence suggested it is an independent biomarker, which is denoted as “F” in the very study. Methods A total of 551 A+T+ individuals from the Alzheimer’s Disease Neuroimaging Initiative database were recruited and then further divided into four groups based on the biomarker positivity as 132 A+T+N−F−, 102 A+T+N−F+, 113 A+T+N+F−, and 204 A+T+N+F+. Frequency distributions of the groups were compared, as well as the clinical progression [measured by the longitudinal changes in cognition and brain structure, and mild cognitive impairment (MCI) to AD dementia conversion] between every pair of F+ and F− groups. Results The prevalence of A+T+N+F+ profile was 66.24% in clinically diagnosed AD dementia patients; similarly, the majority of individuals with reduced FDG-PET were AD dementia subjects. Among the 551 individuals that included, 537 had at least one follow-up (varied from 1 to 8 years). Individuals in F+ groups performed worse and dropped faster in Mini-Mental State Examination scale and had faster shrinking middle temporal lobe than those in F− groups (all p  < 0.05). Moreover, in MCI patients, reduced FDG-PET exerted 2.47 to 4.08-fold risk of AD dementia progression compared with those without significantly impaired FDG-PET (both p  < 0.001). Conclusions Based on the analyses, separating FDG-PET from “N” biomarker to build the ATN(F) system is necessary and well-founded. The analysis from this study could be a complement to the original ATN framework for AD’s biological definition.

PurposeThe advent of immune checkpoint inhibitors (ICIs) has revolutionized the treatment of advanced NSCLC, leading to a string of approvals in recent years. Herein, a narrative review on the role of 18F-fluorodeoxyglucose positron emission tomography/computed tomography (FDG PET/CT) in the ever-evolving treatment landscape of advanced NSCLC is presented.MethodsThis comprehensive review will begin with an introduction into current treatment paradigms incorporating ICIs; the evolution of CT-based criteria; moving onto novel phenomena observed with ICIs and the current state of hybrid imaging for diagnosis, treatment planning, evaluation of treatment efficacy and toxicity in advanced NSCLC, also taking into consideration its limitations and future directions.ConclusionsThe advent of ICIs marks the dawn of a new era bringing forth new challenges particularly vis-à-vis treatment response assessment and observation of novel phenomena accompanied by novel systemic side effects. While FDG PET/CT is widely adopted for tumor volume delineation in locally advanced disease, response assessment to immunotherapy based on current criteria is of high clinical value but has its inherent limitations. In recent years, modifications of established (PET)/CT criteria have been proposed to provide more refined approaches towards response evaluation. Not only a comprehensive inclusion of PET-based response criteria in prospective randomized controlled trials, but also a general harmonization within the variety of PET-based response criteria is pertinent to strengthen clinical implementation and widespread use of hybrid imaging for response assessment in NSCLC.

The International Commission on Radiological Protection has lowered the annual equivalent eye-lens dose to 20 mSv. Although occupational exposure can be high in nuclear medicine (NM) departments, few studies have been conducted regarding eye-lens exposure among NM staff. This study aimed to estimate the annual lens doses of staff in an NM department and identify factors contributing to lens exposure. Four nurses and six radiographers performing positron emission tomography (PET) examinations and four radiographers performing radioisotope (RI) examinations (excluding PET) were recruited for this study. A lens dosimeter was attached near the left eye to measure the 3-mm-dose equivalent; a personal dosimeter was attached to the left side of the neck to measure the 1-cm- and 70-µm-dose equivalents. Measurements were acquired over six months, and the cumulative lens dose was doubled to derive the annual dose. Correlations between the lens and personal-dosimeter doses, between the lens dose and the numbers of procedures, and between the lens dose and the amounts of PET drugs (radiopharmaceuticals) injected were examined. Wilcoxon’s signed-rank test was used to compare lens and personal-dosimeter doses. The estimated annual doses were 0.93 ± 0.13 mSv for PET nurses, 0.71 ± 0.41 mSv for PET radiographers, and 1.10 ± 0.53 mSv for RI radiographers. For PET nurses, but not for PET or RI radiographers, there was a positive correlation between the numbers of procedures and lens doses and between amounts injected and lens doses. There was a significant difference between the lens and personal-dosimeter doses of PET nurses. The use of protective measures, such as shielding, should prevent NM staff from receiving lens doses > 20 mSv/year. However, depending on the height of the protective shield, PET nurses may be unable to assess the lens dose accurately using personal dosimeters.

The present procedural guidelines summarize the current views of the EANM Neuro-Imaging Committee (NIC). The purpose of these guidelines is to assist nuclear medicine practitioners in making recommendations, performing, interpreting, and reporting results of [ 18 F]FDG-PET imaging of the brain. The aim is to help achieve a high-quality standard of [ 18 F]FDG brain imaging and to further increase the diagnostic impact of this technique in neurological, neurosurgical, and psychiatric practice. The present document replaces a former version of the guidelines that have been published in 2009. These new guidelines include an update in the light of advances in PET technology such as the introduction of digital PET and hybrid PET/MR systems, advances in individual PET semiquantitative analysis, and current broadening clinical indications (e.g., for encephalitis and brain lymphoma). Further insight has also become available about hyperglycemia effects in patients who undergo brain [ 18 F]FDG-PET. Accordingly, the patient preparation procedure has been updated. Finally, most typical brain patterns of metabolic changes are summarized for neurodegenerative diseases. The present guidelines are specifically intended to present information related to the European practice. The information provided should be taken in the context of local conditions and regulations.

Fluorine 18 fluorodeoxyglucose ((18)F-FDG) positron emission tomography (PET)/computed tomography (CT) has emerged as a new modality for colorectal cancer (CRC) patients. The aim of this meta-analysis was to assess the diagnostic value of (18)F-FDG PET/CT in detecting local recurrence in patients with CRC. We searched PubMed, Medline, Embase, and ISI databases to collect articles in English that evaluated the diagnostic value of (18)F-FDG PET/CT in patients with CRC. Two reviewers independently assessed the methodological quality of each study using the quality assessment of diagnostic accuracy studies tool. The data were analyzed using Meta-Disc (Version 1.4) and Stata (Version 12.0) software. We estimated the sensitivity, specificity, positive likelihood ratio (PLR), negative likelihood ratio (NLR), diagnostic odds ratio (DOR), and summary receiver operating characteristic (SROC). A total of 26 studies were included. When all the eligible studies included, the pooled sensitivity and specificity for (18)F-FDG PET/CT in detecting CRC were 0.94 (95 % confidence interval [CI] 0.92-0.96) and 0.94 (95 % CI 0.93-0.95), respectively. The pooled PLR and NLR were 14.39 (95 % CI 7.37-28.09) and 0.08 (95 % CI 0.06-0.12), respectively. The DOR was 208.67 (95 % CI 109.56-397.44) and the area under the SROC curve was 0.9776. The overall diagnostic accuracy (Q* index) was 0.9329. (18)F-FDG PET/CT has good diagnostic performance in detecting local recurrence in patients with CRC. Further larger prospective studies are needed to establish its value for detecting local recurrence of CRC cancer patients.

INTRODUCTION Tau pathology impacts neurodegeneration and cognitive decline in Alzheimer's disease (AD), with the dorsal raphe nucleus (DRN) being among the brain regions showing the earliest tau pathology. As a serotonergic hub, DRN activity is altered by selective serotonin reuptake inhibitors (SSRIs), which also have variable effects on cognitive decline and pathology in AD. METHODS We examined N = 191 subjects with baseline 18F‐fluorodeoxyglucose positron emission tomography and plasma biomarker data to study the effects of SSRIs on tau pathology, cognitive decline, and DRN metabolism. RESULTS Plasma phosphorylated tau 181 (p‐tau181) was lower with SSRI use. The effect of SSRIs on cognition varied by cognitive assessment. The DRN was hypometabolic in AD patients relative to healthy controls; however, SSRI use restored the metabolic activity of this region in AD patients. DISCUSSION Long‐term SSRI use may reduce the pathological presentation of AD but has variable effects on cognitive performance. Highlights Tau pathology spreads throughout the brain during AD pathogenesis. The DRN is among the first regions to develop tau pathology during this process. SSRI use restores the metabolic activity of the DRN and reduces plasma p‐tau181.