Articles de revues : « 11C-PiB PET »

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Brown, Desmond, Gobinda Sarkar, Teresa Decklever, Geoffry Curran, Ameet Sarkar, Ann Schmeichel, Suresh Swaminathan et al. « SCIDOT-39. K16ApoE ENHANCES Aβ-ASSOCIATED 11C-PiB DEPOSITION AND PET SIGNAL IN APP/PS1 TRANSGENIC MICE ». Neuro-Oncology 21, Supplement_6 (novembre 2019) : vi279—vi280. http://dx.doi.org/10.1093/neuonc/noz175.1175.

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Abstract OBJECTIVE The K16ApoE peptide enhances delivery of multiple agents across the blood-brain barrier (BBB). Transgenic mouse models are central to elucidating the underlying pathophysiology of Alzheimer’s Disease (AD) and provide a system for evaluating novel therapeutic strategies. PET imaging plays a central clinical role in diagnosing human cases of AD but has had variable performance in mouse models. We investigated the role of K16ApoE to enhance delivery of a radiolabeled PET imaging tracer, 11C-PiB and assess whether this corresponds to improved PET sensitivity in APP/PS1 transgenic mice. METHODS Brain-delivery of 11C-PiB was accomplished by successive injections of K16ApoE and 11C-PiB. Distribution of 11C-PiB to the brain and heart was quantified via dynamic PET/CT imaging and digital autoradiography. RESULTS K16ApoE increased the brain uptake of 11C-PiB in both wild-type (WT) and APP/PS1 mice. Administration of K16ApoE increased the PET standard uptake value of 11C-PiB at 5 minutes in WT mice from 1.132 to 2.963 (p=0.006) and in APP/PS1 mice from 0.842 to 3.268 (p=0.016). Enhancement peaked at 5 minutes. Binding was reversible with similarly increased kinetics in both WT and APP/PS1 mice. The absolute values were higher in APP/PS1 mice suggesting increased retention. The increased retention in APP/PS1 mice was consistent with specific binding to A-beta plaques as unlabeled PiB reduced 11C-PiB signal retention. CONCLUSION K16ApoE mediates enhancement of 11C-PiB signal in APP/PS1 mice brains with increased PET sensitivity. There is increased uptake kinetics in both WT and APP/PS1 mice with specific A-beta plaque binding in the latter. This enhanced delivery of the PET tracer has implications for development and testing of new hypotheses and the efficacy of novel therapeutic paradigms. K16ApoE has potential for improving delivery of several agents across the BBB. This has implication for delivery of diagnostic and therapeutic agents for neurodegenerative and neuro-oncologic diseases.

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Fu, Liping, Linwen Liu, Jinming Zhang, Baixuan Xu, Yong Fan et Jiahe Tian. « Brain Network Alterations in Alzheimer’s Disease Identified by Early-Phase PIB-PET ». Contrast Media & ; Molecular Imaging 2018 (2018) : 1–10. http://dx.doi.org/10.1155/2018/6830105.

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The aim of this study was to identify the brain networks from early-phase 11C-PIB (perfusion PIB, pPIB) data and to compare the brain networks of patients with differentiating Alzheimer’s disease (AD) with cognitively normal subjects (CN) and of mild cognitively impaired patients (MCI) with CN. Forty participants (14 CN, 12 MCI, and 14 AD) underwent 11C-PIB and 18F-FDG PET/CT scans. Parallel independent component analysis (pICA) was used to identify correlated brain networks from the 11C-pPIB and 18F-FDG data, and a two-sample t-test was used to evaluate group differences in the corrected brain networks between AD and CN, and between MCI and CN. Our study identified a brain network of perfusion (early-phase 11C-PIB) that highly correlated with a glucose metabolism (18F-FDG) brain network and colocalized with the default mode network (DMN) in an AD-specific neurodegenerative cohort. Particularly, decreased 18F-FDG uptake correlated with a decreased regional cerebral blood flow in the frontal, parietal, and temporal regions of the DMN. The group comparisons revealed similar spatial patterns of the brain networks derived from the 11C-pPIB and 18F-FDG data. Our findings indicate that 11C-pPIB derived from the early-phase 11C-PIB could provide complementary information for 18F-FDG examination in AD.

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Engler, Henry, Andres Damian et Cecilia Bentancourt. « PET and the multitracer concept in the study of neurodegenerative diseases ». Dementia & ; Neuropsychologia 9, n^o 4 (décembre 2015) : 343–49. http://dx.doi.org/10.1590/1980-57642015dn94000343.

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ABSTRACT The complexity of the pathological reactions of the brain to an aggression caused by an internal or external noxa represents a challenge for molecular imaging. Positron emission tomography (PET) can indicate in vivo,anatomopathological changes involved in the development of different clinical symptoms in patients with neurodegenerative disorders. PET and the multitracer concept can provide information from different systems in the brain tissue building an image of the whole disease. We present here the combination of 18F-flourodeoxyglucose (FDG) and N-[11C-methyl]-L-deuterodeprenyl (DED), FDG and N-[11C-methyl] 2-(4'-methylaminophenyl)-6-hydroxybenzothiazole (PIB), PIB and L-[11C]-3'4-Dihydrophenylalanine (DOPA) and finally PIB and [15O]H2O.

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Veronese, Mattia, Benedetta Bodini, Daniel García-Lorenzo, Marco Battaglini, Salvatore Bongarzone, Claude Comtat, Michel Bottlaender, Bruno Stankoff et Federico E. Turkheimer. « Quantification of [11C]PIB PET for Imaging Myelin in the Human Brain : A Test—Retest Reproducibility Study in High-Resolution Research Tomography ». Journal of Cerebral Blood Flow & ; Metabolism 35, n^o 11 (10 juin 2015) : 1771–82. http://dx.doi.org/10.1038/jcbfm.2015.120.

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An accurate in vivo measure of myelin content is essential to deepen our insight into the mechanisms underlying demyelinating and dysmyelinating neurological disorders, and to evaluate the effects of emerging remyelinating treatments. Recently [11C]PIB, a positron emission tomography (PET) tracer originally conceived as a beta-amyloid marker, has been shown to be sensitive to myelin changes in preclinical models and humans. In this work, we propose a reference-region methodology for the voxelwise quantification of brain white-matter (WM) binding for [11C]PIB. This methodology consists of a supervised procedure for the automatic extraction of a reference region and the application of the Logan graphical method to generate distribution volume ratio (DVR) maps. This approach was assessed on a test–retest group of 10 healthy volunteers using a high-resolution PET tomograph. The [11C]PIB PET tracer binding was shown to be up to 23% higher in WM compared with gray matter, depending on the image reconstruction. The DVR estimates were characterized by high reliability (outliers < 1%) and reproducibility (intraclass correlation coefficient (ICC) > 0.95). [11C]PIB parametric maps were also found to be significantly correlated ( R2 > 0.50) to mRNA expressions of the most represented proteins in the myelin sheath. On the contrary, no correlation was found between [11C]PIB imaging and nonmyelin-associated proteins.

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Knezevic, Dunja, Nicolaas Paul LG Verhoeff, Sina Hafizi, Antonio P. Strafella, Ariel Graff-Guerrero, Tarek Rajji, Bruce G. Pollock, Sylvain Houle, Pablo M. Rusjan et Romina Mizrahi. « Imaging microglial activation and amyloid burden in amnestic mild cognitive impairment ». Journal of Cerebral Blood Flow & ; Metabolism 38, n^o 11 (14 novembre 2017) : 1885–95. http://dx.doi.org/10.1177/0271678x17741395.

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Amnestic mild cognitive impairment (aMCI) is defined as a transitional state between normal aging and Alzheimer’s disease (AD). Given the replicated finding of increased microglial activation in AD, we sought to investigate whether microglial activation is also elevated in aMCI and whether it is related to amyloid beta (Aβ) burden in-vivo . Eleven aMCI participants and 14 healthy volunteers completed positron emission tomography (PET) scans with [18F]-FEPPA and [11C]-PIB. Given the known sensitivity in affinity of second-generation TSPO radioligands, participants were genotyped for the TSPO polymorphism and only high-affinity binders were included. Dynamic [18F]-FEPPA PET images were analyzed using the 2-tissue compartment model with arterial plasma input function. Additionally, a supplementary method, the standardized uptake value ratio (SUVR), was explored. [11C]-PIB PET images were analyzed using the Logan graphical method. aMCI participants had significantly higher [11C]-PIB binding in the cortical regions. No significant differences in [18F]-FEPPA binding were observed between aMCI participants and healthy volunteers. In the aMCI group, [18F]-FEPPA and [11C]-PIB bindings were correlated in the hippocampus. There were no correlations between our PET measures and cognition. Our findings demonstrate that while Aβ burden is evident in the aMCI stage, microglial activation may not be present.

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Rodda, J., A. Okello, P. Edison, T. Dannhauser, D. J. Brooks et Z. Walker. « 11C-PIB PET in subjective cognitive impairment ». European Psychiatry 25, n^o 2 (mars 2010) : 123–25. http://dx.doi.org/10.1016/j.eurpsy.2009.07.011.

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AbstractPeople with Subjective Cognitive Impairment (SCI) may be at increased risk of dementia. In this study we examined amyloid load in 5 SCI subjects and 14 controls using PIB PET scanning. One SCI subject had significantly increased PIB retention in the cortical areas of interest. Larger, longitudinal studies are indicated.

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Okazawa, Hidehiko, Masamichi Ikawa, Tetsuya Tsujikawa, Akira Makino, Tetsuya Mori, Yasushi Kiyono et Hirotaka Kosaka. « Noninvasive Measurement of [11C]PiB Distribution Volume Using Integrated PET/MRI ». Diagnostics 10, n^o 12 (24 novembre 2020) : 993. http://dx.doi.org/10.3390/diagnostics10120993.

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A noninvasive image-derived input function (IDIF) method using PET/MRI was applied to quantitative measurements of [11C] Pittsburgh compound-B (PiB) distribution volume (DV) and compared with other metrics. Fifty-three patients suspected of early dementia (71 ± 11 y) underwent 70 min [11C]PiB PET/MRI. Nineteen of them (68 ± 11 y) without head motion during the scan were enrolled in this study and compared with 16 age-matched healthy controls (CTL: 68 ± 11 y). The dynamic frames reconstructed from listmode PET data were used for DV calculation. IDIF with metabolite correction was applied to the Logan plot method, and DV was normalized into DV ratio (DVR) images using the cerebellar reference (DVRL). DVR and standardized uptake value ratio (SUVR) images were also calculated using the reference tissue graphical method (DVRr) and the 50–70 min static data with cerebellar reference, respectively. Cortical values were compared using the 3D-T1WI MRI segmentation. All patients were assigned to the early Alzheimer’s disease (eAD) group because of positive [11C]PiB accumulation. The correlations of regional values were better for DVRL vs. DVRr (r2 = 0.97) than for SUVR vs. DVRr (r2 = 0.88). However, all metrics clearly differentiated eAD from CTL with appropriate thresholds. Noninvasive quantitative [11C]PiB PET/MRI measurement provided equivalent DVRs with the two methods. SUVR images showed acceptable results despite inferior variability and image quality to DVR images.

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Hosokawa, Chisa, Kazunari Ishii, Tomoko Hyodo, Kenta Sakaguchi, Kimio Usami, Kenji Shimamoto, Yuzuru Yamazoe et al. « Investigation of 11C-PiB equivocal PET findings ». Annals of Nuclear Medicine 29, n^o 2 (6 novembre 2014) : 164–69. http://dx.doi.org/10.1007/s12149-014-0924-8.

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Grecchi, Elisabetta, Mattia Veronese, Benedetta Bodini, Daniel García-Lorenzo, Marco Battaglini, Bruno Stankoff et Federico E. Turkheimer. « Multimodal partial volume correction : Application to [11C]PIB PET/MRI myelin imaging in multiple sclerosis ». Journal of Cerebral Blood Flow & ; Metabolism 37, n^o 12 (1 juin 2017) : 3803–17. http://dx.doi.org/10.1177/0271678x17712183.

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The [11C]PIB PET tracer, originally developed for amyloid imaging, has been recently repurposed to quantify demyelination and remyelination in multiple sclerosis (MS). Myelin PET imaging, however, is limited by its low resolution that deteriorates the quantification accuracy of white matter (WM) lesions. Here, we introduce a novel partial volume correction (PVC) method called Multiresolution–Multimodal Resolution-Recovery (MM-RR), which uses the wavelet transform and a synergistic statistical model to exploit MRI structural images to improve the resolution of [11C]PIB PET myelin imaging. MM-RR performance was tested on a phantom acquisition and in a dataset comprising [11C]PIB PET and MR T1- and T2-weighted images of 8 healthy controls and 20 MS patients. For the control group, the MM-RR PET images showed an average increase of 5.7% in WM uptake while the grey-matter (GM) uptake remained constant, resulting in +31% WM/GM contrast. Furthermore, MM-RR PET binding maps correlated significantly with the mRNA expressions of the most represented proteins in the myelin sheath (R2 = 0.57 ± 0.09). In the patient group, MM-RR PET images showed sharper lesion contours and significant improvement in normal-appearing tissue/WM-lesion contrast compared to standard PET (contrast improvement > +40%). These results were consistent with MM-RR performances in phantom experiments.

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Baron, Jean-Claude, Karim Farid, Eamon Dolan, Guillaume Turc, Siva T. Marrapu, Eoin O'Brien, Franklin I. Aigbirhio et al. « Diagnostic Utility of Amyloid PET in Cerebral Amyloid Angiopathy-Related Symptomatic Intracerebral Hemorrhage ». Journal of Cerebral Blood Flow & ; Metabolism 34, n^o 5 (12 mars 2014) : 753–58. http://dx.doi.org/10.1038/jcbfm.2014.43.

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By detecting β-amyloid ( Aβ) in the wall of cortical arterioles, amyloid positron emission tomography (PET) imaging might help diagnose cerebral amyloid angiopathy (CAA) in patients with lobar intracerebral hemorrhage (I-ICH). No previous study has directly assessed the diagnostic value of 11-Pittsburgh compound B (PiB) PET in probable CAA-related I-ICH against healthy controls (HCs). 11C-PiB-PET and magnetic resonance imaging (MRI) including T2* were obtained in 11 nondemented patients fulfilling the Boston criteria for probable CAA-related symptomatic I-ICH (sl-ICH) and 20 HCs without cognitive complaints or impairment. After optimal spatial normalization, cerebral spinal fluid (CSF)-corrected PiB distribution volume ratios (DVRs) were obtained. There was no significant difference in whole cortex or regional DVRs between CAA patients and age-matched HCs. The whole cortex DVR was above the 95% confidence limit in 4/9 HCs and 10/11 CAA patients (sensitivity = 91%, specificity = 55%). Region/frontal or occipital ratios did not have better discriminative value. Similar but less accurate results were found using visual analysis. In patients with sl-ICH, 11C-PiB-PET has low specificity for CAA due to the frequent occurrence of high 11C-PiB uptake in the healthy elderly reflecting incipient Alzheimer's disease (AD), which might also be present in suspected CAA. However, a negative PiB scan rules out CAA with excellent sensitivity, which has clinical implications for prognostication and selection of candidates for drug trials.

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Shirvan, Julia, Nathan Clement, Rong Ye, Samantha Katz, Aaron Schultz, Keith A. Johnson, Teresa Gomez-Isla, Matthew Frosch, John H. Growdon et Stephen N. Gomperts. « Neuropathologic correlates of amyloid and dopamine transporter imaging in Lewy body disease ». Neurology 93, n^o 5 (26 juin 2019) : e476-e484. http://dx.doi.org/10.1212/wnl.0000000000007855.

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ObjectiveTo develop imaging biomarkers of diseases in the Lewy body spectrum and to validate these markers against postmortem neuropathologic findings.MethodsFour cognitively normal participants with Parkinson disease (PD), 4 with PD with cognitive impairments, and 10 with dementia with Lewy bodies underwent amyloid imaging with [11C]Pittsburgh compound B (PiB) and dopamine transporter (DAT) imaging with [11C]Altropane. All 18 had annual neurologic examinations. All cognitively normal participants with PD developed cognitive impairment before death. Neuropathologic examinations assessed and scored Braak Lewy bodies, Thal distribution of amyloid, Consortium to Establish a Registry for Alzheimer's Disease neuritic amyloid plaques, Braak neurofibrillary tangles, and cerebral amyloid angiopathy, as well as total amyloid plaque burden in the superior frontal, superior parietal, occipital, and inferior temporal cortical regions. PET data were expressed as the standardized uptake value ratio with cerebellar reference. Analyses accounted for the interval between imaging and autopsy.ResultsAll 18 patients met neuropathologic criteria for Lewy body disease; the DAT concentration was low in each case. All patients with elevated [11C]PiB retention measured in a neocortical aggregate had β-amyloid deposits at autopsy. [11C]PiB retention significantly correlated with neuritic plaque burden and with total plaque burden. [11C]PiB retention also significantly correlated with the severity of both Braak stages of neurofibrillary tangle and Lewy body scores. Neuritic plaque burden was significantly associated with neurofibrillary tangle pathology.ConclusionAntemortem [11C]Altropane PET is a sensitive measure of substantia nigra degeneration. [11C]PiB scans accurately reflect cortical amyloid deposits seen at autopsy. These findings support the use of molecular imaging in the evaluation of patients with Lewy body diseases.

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Nakaizumi, K., T. Terada, E. Yoshikawa, A. Kakimoto, I. Takashi, I. Suzuki, B. Tomoyasu et al. « Implication of altered α7 nicotinic receptors and amyloid deposition in the Alzheimer's brain ». European Psychiatry 33, S1 (mars 2016) : S199. http://dx.doi.org/10.1016/j.eurpsy.2016.01.468.

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IntroductionBrain amyloid-β protein (Aβ) deposition is a key pathology of Alzheimer's disease (AD). Cholinergic degeneration, including reductions in α7 nicotinic acetylcholine receptors (α7-nAChR), is also known as a pathophysiology of AD. Recent imaging studies have shown cognitively normal subjects with Aβ depositions, indicating a missing link between Aβ deposition and cognitive decline.ObjectivesTo clarify relationships among the Aβ burden, α7-nAChR availability, and cognitive declines in AD.AimsTo measure brain Aβ deposition and α7-nAChR availability in the same patients with AD using positron emission tomography (PET).MethodsTwenty AD patients and age-matched 20 healthy adults were studied. The α7-nAChR availability and Aβ deposition were evaluated using PET with [11C]MeQAA and [11C]PIB, respectively. Levels of specific binding were estimated by a simplified reference tissue method (BPND) for [11C]MeQAA and a tissue ratio method (SUVR) for using [11C]PIB. The values were compared with clinical measures of various cognitive functions using regions of interest (ROIs)-based and statistical parametric mapping (SPM) analyses.Results[11C]MeQAA BPND levels were extensively lower in the cholinergic projection regions of AD. There was a significant negative correlation between [11C]PIB SUVR and [11C]MeQAA BPND in the nucleus basalis of Mynert (NBM). The NBM [11C]PIB SUVR was negatively correlated with the [11C]MeQAA BPND level in the anterior and posterior cingulate cortices, whereas the relation within the same region showed weak correlation. Also we found significant correlation between cognitive decline and [11C]MeQAA BPND levels in the NBM.ConclusionsAβ deposition-linked α7-nAChR dysfunction may account for cognitive decline in AD.Disclosure of interestThe authors have not supplied their declaration of competing interest.

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Heeman, Fiona, Janine Hendriks, Isadora Lopes Alves, Nelleke Tolboom, Bart N. M. van Berckel, Maqsood Yaqub et Adriaan A. Lammertsma. « Test-Retest Variability of Relative Tracer Delivery Rate as Measured by [11C]PiB ». Molecular Imaging and Biology 23, n^o 3 (21 avril 2021) : 335–39. http://dx.doi.org/10.1007/s11307-021-01606-z.

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Abstract Purpose Moderate-to-high correlations have been reported between the [11C]PiB PET-derived relative tracer delivery rate R1 and relative CBF as measured using [15O]H2O PET, supporting its use as a proxy of relative CBF. As longitudinal PET studies become more common for measuring treatment efficacy or disease progression, it is important to know the intrinsic variability of R1. The purpose of the present study was to determine this through a retrospective data analysis. Procedures Test-retest data belonging to twelve participants, who underwent two 90 min [11C]PiB PET scans, were retrospectively included. The voxel-based implementation of the two-step simplified reference tissue model with cerebellar grey matter as reference tissue was used to compute R1 images. Next, test-retest variability was calculated, and test and retest R1 measures were compared using linear mixed effect models and a Bland-Altman analysis. Results Test-retest variability was low across regions (max. 5.8 %), and test and retest measures showed high, significant correlations (R2=0.92, slope=0.98) and a negligible bias (0.69±3.07 %). Conclusions In conclusion, the high precision of [11C]PiB R1 suggests suitable applicability for cross-sectional and longitudinal studies.

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Oliveira, Francisco P. M., Ana Paula Moreira, Alexandre de Mendonça, Ana Verdelho, Carolina Xavier, Dalila Barroca, Joana Rio et al. « Can 11C-PiB-PET Relative Delivery R1 or 11C-PiB-PET Perfusion Replace 18F-FDG-PET in the Assessment of Brain Neurodegeneration ? » Journal of Alzheimer's Disease 65, n^o 1 (7 août 2018) : 89–97. http://dx.doi.org/10.3233/jad-180274.

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Gao, Zhong-Bao, Wei Wang, Xing-Li Zhao, Tong Chen, Li-Ping Fu, Bai-Xuan Xu et Zhen-Fu Wang. « Multi-modality molecular imaging characteristics of dementia with Lewy bodies ». Journal of International Medical Research 46, n^o 6 (5 avril 2018) : 2317–26. http://dx.doi.org/10.1177/0300060518764749.

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Objective Dementia with Lewy bodies (DLB) is a common type of neurodegenerative dementia. Molecular neuroimaging using dopamine transporter (DaT), Pittsburgh compound B (PIB), and fluorodeoxyglucose (FDG) positron emission tomography (PET) has advantages in detecting dopaminergic neuron loss, abnormal amyloid β-protein deposition, and glucose metabolism changes in patients with neurodegenerative disorders. However, the multi-modality molecular imaging features of patients with DLB have rarely been reported. Methods Five patients with a probable diagnosis of DLB were enrolled. PET/magnetic resonance imaging was performed with three tracers: 11C-β-CFT, 11C-PIB, and 18F-FDG. Clinical and imaging characteristics were analyzed. Results All patients with DLB showed reduced uptake in the bilateral putamen on DaT PET, increased uptake throughout the cerebral cortex on PIB PET, and intact metabolism of the posterior cingulate gyrus on FDG PET. Conclusion Multimodal molecular imaging is helpful for early diagnosis of DLB. Studies with larger sample sizes are needed to confirm the molecular imaging differences between DLB and Alzheimer’s disease and Parkinson’s disease dementia.

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Ng, Steven Y., Victor L. Villemagne, Sylvia Gong, Graeme O’Keefe, Henri Tochon-Danguy, Uwe Ackermann et Christopher C. Rowe. « 101. Brain Amyloid Imaging with 11C-PIB PET ». Journal of Clinical Neuroscience 16, n^o 3 (mars 2009) : 462. http://dx.doi.org/10.1016/j.jocn.2008.07.002.

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Shinotoh, Hitoshi, Hitoshi Shimada, Yasumasa Kokubo, Kenji Tagai, Fumitoshi Niwa, Soichiro Kitamura, Hironobu Endo et al. « Tau imaging detects distinctive distribution of tau pathology in ALS/PDC on the Kii Peninsula ». Neurology 92, n^o 2 (7 décembre 2018) : e136-e147. http://dx.doi.org/10.1212/wnl.0000000000006736.

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ObjectiveTo characterize the distribution of tau pathology in patients with amyotrophic lateral sclerosis/parkinsonism dementia complex on the Kii Peninsula (Kii ALS/PDC) by tau PET using [11C]PBB3 as ligand.MethodsThis is a cross-sectional study of 5 patients with ALS/PDC and one asymptomatic participant with a dense family history of ALS/PDC from the Kii Peninsula who took part in this study. All were men, and their age was 76 ± 8 (mean ± SD) years. Thirteen healthy men (69 ± 6 years) participated as healthy controls (HCs). Dynamic PET scans were performed following injection of [11C]PBB3, and parametric PET images were generated by voxel-by-voxel calculation of binding potential (BP*ND) using a multilinear reference tissue model. [11C] Pittsburgh compound B (PiB) PET, MRI, and cognitive tests were also performed.ResultsA voxel-based comparison of [11C]PBB3 BP*ND illustrated PET-detectable tau deposition in the cerebral cortex and white matter, and pontine basis including the corticospinal tract in Kii ALS/PDC patients compared with HCs (uncorrected p < 0.05). Group-wise volume of interest analysis of [11C]PBB3 BP*ND images showed increased BP*ND in the hippocampus and in frontal and parietal white matters of Kii ALS/PDC patients relative to HCs (p < 0.05, Holm-Sidak multiple comparisons test). BP*ND in frontal, temporal, and parietal gray matters correlated with Mini-Mental State Examination scores in Kii ALS/PDC patients (p < 0.05). All Kii ALS/PDC patients were negative for [11C]PiB (β-amyloid) except one with marginal positivity.Conclusion[11C]PBB3 PET visualized the characteristic topography of tau pathology in Kii ALS/PDC, corresponding to clinical phenotypes of this disease.

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Ikoma, Yoko, Paul Edison, Anil Ramlackhansingh, David J. Brooks et Federico E. Turkheimer. « Reference Region Automatic Extraction in Dynamic [11C]PIB ». Journal of Cerebral Blood Flow & ; Metabolism 33, n^o 11 (7 août 2013) : 1725–31. http://dx.doi.org/10.1038/jcbfm.2013.133.

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The positron emission tomography (PET) radiotracer [11C]Pittsburgh Compound B (PIB) is a marker of amyloid plaque deposition in brain, and binding potential is usually quantified using the cerebellum as a reference where the specific binding is negligible. The use of the cerebellum as a reference, however, has been questioned by the reported cerebellar [11C]PIB retention in familial Alzheimer's disease (AD) subjects. In this work, we developed a supervised clustering procedure for the automatic extraction of a reference region in [11C]PIB studies. Supervised clustering models each gray matter voxel as the linear combination of three predefined kinetic classes, normal and lesion gray matter, and blood pool, and extract reference voxels in which the contribution of the normal gray matter class is high. In the validation with idiopathic AD subjects, supervised clustering extracted reference voxels mostly in the cerebellum that indicated little specific [11C]PIB binding, and total distribution volumes of the extracted region were lower than those of the cerebellum. Next, the methodology was applied to the familial AD cohort where the cerebellar amyloid load had been demonstrated previously, resulting in higher binding potential compared with that obtained with the cerebellar reference. The supervised clustering method is a useful tool for the accurate quantification of [11C]PIB studies.

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Zoufal, Viktoria, Severin Mairinger, Markus Krohn, Thomas Wanek, Thomas Filip, Michael Sauberer, Johann Stanek, Claudia Kuntner, Jens Pahnke et Oliver Langer. « Measurement of cerebral ABCC1 transport activity in wild-type and APP/PS1-21 mice with positron emission tomography ». Journal of Cerebral Blood Flow & ; Metabolism 40, n^o 5 (13 juin 2019) : 954–65. http://dx.doi.org/10.1177/0271678x19854541.

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Previous data suggest a possible link between multidrug resistance-associated protein 1 (ABCC1) and brain clearance of beta-amyloid (Aβ). We used PET with 6-bromo-7-[11C]methylpurine ([11C]BMP) to measure cerebral ABCC1 transport activity in a beta-amyloidosis mouse model (APP/PS1-21) and in wild-type mice aged 50 and 170 days, without and with pretreatment with the ABCC1 inhibitor MK571. One hundred seventy days-old-animals additionally underwent [11C]PiB PET scans to measure Aβ load. While baseline [11C]BMP PET scans detected no differences in the elimination slope of radioactivity washout from the brain (kelim) between APP/PS1-21 and wild-type mice of both age groups, PET scans after MK571 pretreatment revealed significantly higher kelim values in APP/PS1-21 mice than in wild-type mice aged 170 days, suggesting increased ABCC1 activity. The observed increase in kelim occurred across all investigated brain regions and was independent of the presence of Aβ plaques measured with [11C]PiB. Western blot analysis revealed a trend towards increased whole brain ABCC1 levels in 170 days-old-APP/PS1-21 mice versus wild-type mice and a significant positive correlation between ABCC1 levels and kelim. Our data point to an upregulation of ABCC1 in APP/PS1-21 mice, which may be related to an induction of ABCC1 in astrocytes as a protective mechanism against oxidative stress.

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Reesink, F. E., D. Vállez García, C. A. Sánchez-Catasús, D. E. Peretti, A. T. Willemsen, R. Boellaard, S. K. Meles et al. « Crossed Cerebellar Diaschisis in Alzheimer’s Disease ». Current Alzheimer Research 15, n^o 13 (29 octobre 2018) : 1267–75. http://dx.doi.org/10.2174/1567205015666180913102615.

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Background: We describe the phenomenon of crossed cerebellar diaschisis (CCD) in four subjects diagnosed with Alzheimer’s disease (AD) according to the National Institute on Aging - Alzheimer Association (NIA-AA) criteria, in combination with 18F-FDG PET and 11C-PiB PET imaging. Methods: 18F-FDG PET showed a pattern of cerebral metabolism with relative decrease most prominent in the frontal-parietal cortex of the left hemisphere and crossed hypometabolism of the right cerebellum. 11C-PiB PET showed symmetrical amyloid accumulation, but a lower relative tracer delivery (a surrogate of relative cerebral blood flow) in the left hemisphere. CCD is the phenomenon of unilateral cerebellar hypometabolism as a remote effect of supratentorial dysfunction of the brain in the contralateral hemisphere. The mechanism implies the involvement of the cortico-ponto-cerebellar fibers. The pathophysiology is thought to have a functional or reversible basis but can also reflect in secondary morphologic change. CCD is a well-recognized phenomenon, since the development of new imaging techniques, although scarcely described in neurodegenerative dementias. Results: To our knowledge this is the first report describing CCD in AD subjects with documentation of both 18F-FDG PET and 11C-PiB PET imaging. CCD in our subjects was explained on a functional basis due to neurodegenerative pathology in the left hemisphere. There was no structural lesion and the symmetric amyloid accumulation did not correspond with the unilateral metabolic impairment. Conclusion: This suggests that CCD might be caused by non-amyloid neurodegeneration. The pathophysiological mechanism, clinical relevance and therapeutic implications of CCD and the role of the cerebellum in AD need further investigation.

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Yamamoto, Yuka, Yukito Maeda, Nobuyuki Kawai, Nobuyuki Kudomi et Yoshihiro Nishiyama. « Unexpected Finding of Cerebral Meningioma on 11C-PiB PET ». Clinical Nuclear Medicine 38, n^o 4 (avril 2013) : 292–93. http://dx.doi.org/10.1097/rlu.0b013e3182817c8f.

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Sinha, N., A. Zhou, Y. Li, N. Joseph-Mathurin, C. Xiong, JC Morris, R. Bateman, TL Benzinger et NJ Cairns. « Stereologic measures of beta-amyloid load in postmortem autosomal dominant Alzheimer disease brain validate PiB-PET as a useful biomarker ». Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 46, s2 (septembre 2019) : S60—S61. http://dx.doi.org/10.1017/cjn.2019.257.

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In vivo positron emission tomography (PET) using [C11]-labeled Pittsburgh Compound B ([C11]PiB) has previously been shown to detect amyloid-β (Aβ) in late-onset Alzheimer disease (LOAD) brain; however, the sensitivity of this technique for detecting β-amyloidosis in autosomal dominant Alzheimer disease (ADAD) has not been systematically investigated. To validate [C11]PiB PET as a useful biomarker of β-amyloidosis, we measured the cortical and regional standardized uptake value ratios (SUVRs) in 16 ADAD and 15 LOAD cases and compared them with histopathologic measures of β-amyloidosis in postmortem brain. The PiB-PET data were obtained between 40–70 min after bolus injection of ∼15 mCi of [11C]PiB. MRI and PiB-PET images were co-registered and SUVRs were generated for several brain regions. Using Aβ immunohistochemistry (10D5, Eli Lilly), the burden of Aβ plaques was quantified in 16 regions of interest using an area fraction fractionator probe (Stereo Investigator, MicroBrightfield, VT). There were regional variations in Aβ plaque burden with highest densities observed in the neocortical areas and the striatum. On spearman correlations, in vivo PiB-PET correlated with postmortem Aβ plaque burden in both LOAD and ADAD, with strongest correlations seen in neocortical areas. In summary, [C11]PiB-PET has utility as a biomarker in both ADAD and LOAD.LEARNING OBJECTIVESThis presentation will enable the learner to:1.Discuss how PET-PiB beta-amyloid imaging is used as a potential biomarker of Alzheimer disease (AD)2.Correlate postmortem neuropathologic evidence of beta-amyloidosis with PET-PiB data, and learn that PET-PiB is a potentially useful tool to detect beta-amyloidosis in presymptomatic and symptomatic individuals

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Grimmer, Timo, Panagiotis Alexopoulos, Amalia Tsolakidou, Liang-Hao Guo, Gjermund Henriksen, Behrooz H. Yousefi, Hans Förstl et al. « Cerebrospinal Fluid BACE1 Activity and Brain Amyloid Load in Alzheimer's Disease ». Scientific World Journal 2012 (2012) : 1–6. http://dx.doi.org/10.1100/2012/712048.

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The secretase BACE1 is fundamentally involved in the development of cerebral amyloid pathology in Alzheimer's disease (AD). It has not been studied so far to what extent BACE1 activity in cerebrospinal fluid (CSF) mirrors in vivo amyloid load in AD. We explored associations between CSF BACE1 activity and fibrillar amyloid pathology as measured by carbon-11-labelled Pittsburgh Compound B positron emission tomography ([11C]PIB PET). [11C]PIB and CSF studies were performed in 31 patients with AD. Voxel-based linear regression analysis revealed significant associations between CSF BACE1 activity and [11C]PIB tracer uptake in the bilateral parahippocampal region, the thalamus, and the pons. Our study provides evidence for a brain region-specific correlation between CSF BACE1 activity and in-vivo fibrillar amyloid pathology in AD. Associations were found in areas close to the brain ventricles, which may have important implications for the use of BACE1 in CSF as a marker for AD pathology and for antiamyloid treatment monitoring.

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Rodda, J., T. Dannhauser, D. Cutinha, A. Okello, S. Shergill, D. Brooks et Z. Walker. « Subjective Cognitive Impairment : Functional MRI During Divided Attention and Measurement of Amyloid Load Using 11C-PIB PET ». European Psychiatry 24, S1 (janvier 2009) : 1. http://dx.doi.org/10.1016/s0924-9338(09)70375-x.

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Background:Evidence suggests that healthy older adults with subjective memory complaints are at increased risk of dementia. Subjective Cognitive Impairment (SCI) may precede Mild Cognitive Impairment (MCI) in the clinical continuum of Alzheimer's disease (AD). Attentional deficits may be present early in AD, and associated functional changes have been reported in both MCI and AD. In the present study, activation during divided attention in SCI subjects was investigated using functional magnetic resonance imaging (fMRI). Additionally, amyloid uptake was investigated using 11C-PIB with positron emission tomography (PET).Methods:Brain activation in 11 SCI subjects and 10 controls was compared during a divided attention task using fMRI. Additionally, five SCI subjects and 14 cognitively normal healthy controls underwent 11C-PIB PET scanning. Criteria for diagnosis of SCI were:1.self-reported memory complaints,2.objectively normal cognition on detailed neurocognitive testing,3.absence of psychiatric or causative physical illness,4.normal activities of daily living and5.absence of MCI or dementia.Results:There were no differences in performance between SCI and control groups in terms of cognitive or behavioural measures. However, SCIs had increased activation in left medial temporal lobe, and bilateral thalamus, posterior cingulate and caudate. One SCI subject and one control subject had a pattern of 11C-PIB uptake similar to that seen in AD.Conclusions:The activation changes identified in SCI may relate to compensatory increased activation in the face of early AD pathology. Larger, longitudinal studies are needed to determine the extent and significance of PIB uptake in SCI.

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Takenoshita, Naoto, Raita Fukasawa, Yusuke Ogawa, Soichiro Shimizu, Takahiko Umahara, Kenji Ishii, Hitoshi Shimada, Makoto Higuchi, Tetsuya Suhara et Haruo Hanyu. « Amyloid and Tau Positron Emission Tomography in Suggested Diabetesrelated Dementia ». Current Alzheimer Research 15, n^o 11 (7 septembre 2018) : 1062–69. http://dx.doi.org/10.2174/1567205015666180709113338.

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Background: Type 2 diabetes mellitus (DM) has been shown to increase the risk for cognitive decline and dementia, such as Alzheimer disease (AD) and vascular dementia (VaD). In addition to AD and VaD, there may be a dementia subgroup associated with specific DM-related metabolic abnormalities rather than AD pathology or cerebrovascular disease, referred to as diabetes-related dementia (DrD). Method: We studied 11C-PiB and 11C-PBB3 positron emission tomography (PET) in 31 subjects with DrD and 5 subjects with AD associated with DM to assess amyloid and tau deposits in the brain. Results: All subjects with AD showed both positive PiB and PBB3. However, only 12 out of 31 subjects (39%) with DrD showed positive PiB, whereas 17 out of 21 subjects (81%) who underwent PBB3 PET showed positive PBB3. Depending on the positivity of PiB and PBB3, we classified 21 subjects into a negative PiB and a positive PBB3 pattern (11 cases, 52%), indicating tauopathy, a positive PiB and a positive PBB3 pattern (6 cases, 29%), indicating AD pathology, or a negative PiB and a negative PBB3 pattern (4 cases, 19%). Among 11 subjects showing a negative PiB and a positive PBB3 pattern, there were 2 PBB3 deposit patterns, including the medial temporal lobe only and extensive neocortex beyond the medial temporal lobe. Conclusion: DrD showed variable amyloid and tau accumulation patterns in the brain. DrD may be associated predominantly with tau pathology, in addition to AD pathology and non-amyloid/non-tau neuronal damage due to DM-related metabolic abnormalities.

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Ylä-Herttuala, Salla, Mikko Hakulinen, Pekka Poutiainen, Tiina M. Laitinen, Anne M. Koivisto, Anne M. Remes, Merja Hallikainen et al. « Severe Obstructive Sleep Apnea and Increased Cortical Amyloid-β Deposition ». Journal of Alzheimer's Disease 79, n^o 1 (5 janvier 2021) : 153–61. http://dx.doi.org/10.3233/jad-200736.

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Background: The suggested association between severe obstructive sleep apnea (OSA) and risk of Alzheimer’s disease (AD) needs further study. Only few recent reports exist on associations between brain amyloid-β (Aβ) burden and severe OSA in middle-aged patients. Objective: Examine the possible presence of cortical Aβ accumulation in middle-aged patients with severe OSA. Methods: We performed detailed multimodal neuroimaging in 19 cognitive intact patients (mean 44.2 years) with severe OSA (Apnea-Hypopnea Index >30 h–1). Known etiological factors for possible Aβ accumulation were used as exclusion criteria. Aβ uptake was studied with [11C]-PiB-PET, glucose metabolism with [18F]-FDG-PET, and structural imaging with 3.0T MRI. Results: When analyzed individually, in [11C]-PiB-PET a substantial number (∼32%) of the patients exhibited statistically significant evidence of increased cortical Aβ uptake based on elevated regional Z-score values, mostly seen bilaterally in the precuneus and posterior cingulum regions. Cortical glucose hypometabolism in [18F]-FDG-PET was seen in two patients. MRI did not show structural changes suggestive of AD-related pathology. Conclusion: Increased [11C]-PiB uptake was seen in middle-aged cognitively intact patients with severe OSA. These findings are similar to those described in cognitive unimpaired older OSA patients. The changes in cortical Aβ uptake suggest that severe OSA itself may predispose to alterations related to AD already in middle-age. Aβ clearance may be compromised without simultaneous evidence of metabolic or structural alterations. The results emphasize the importance of early diagnostics and proper treatment of severe OSA in cognitively intact middle-aged subjects, possibly diminishing the individual risk for later cognitive dysfunction.

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Edison, Paul, Hilary A. Archer, Alexander Gerhard, Rainer Hinz, Nicola Pavese, Federico E. Turkheimer, Alexander Hammers et al. « Microglia, amyloid, and cognition in Alzheimer's disease : An [11C](R)PK11195-PET and [11C]PIB-PET study ». Neurobiology of Disease 32, n^o 3 (décembre 2008) : 412–19. http://dx.doi.org/10.1016/j.nbd.2008.08.001.

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Mariani, Francesca, Andrés Damian, Pablo Duarte, Stephanie Pino, Sergio Dansilio et Rodolfo Ferrando. « Corticobasal syndrome as a focal variant of Alzheimer’s disease ». Journal of Applied Cognitive Neuroscience 3, n^o 2 (11 décembre 2022) : e00284513. http://dx.doi.org/10.17981/jacn.3.2.2022.06.

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We present A 60-year-old woman with a 2-year history of progressive anterograde memory deficit, with a A 18F-FDG PET/CT and 11C-PIB PET/CT studies performed. In the follow-up she presented a typical corticobasal syndrome with extrapyramidal signs and left superior limb dystonia. These clinical and imaging features are consistent with a focal presentation of AD.

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Antoni, Gunnar, et Per Westermark. « 11C-PIB and PET for the detection of cardiac amyloid ». Imaging in Medicine 5, n^o 5 (octobre 2013) : 395–98. http://dx.doi.org/10.2217/iim.13.43.

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Kiddle, Steven John, Madhav Thambisetty, Andrew Simmons, Joanna Riddoch-Contreras, Abdul Hye, Eric Westman, Ian Pike et al. « Plasma Based Markers of [11C] PiB-PET Brain Amyloid Burden ». PLoS ONE 7, n^o 9 (24 septembre 2012) : e44260. http://dx.doi.org/10.1371/journal.pone.0044260.

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Villemagne, V. L., C. A. McLean, K. Reardon, A. Boyd, V. Lewis, G. Klug, G. Jones et al. « 11C-PiB PET studies in typical sporadic Creutzfeldt-Jakob disease ». Journal of Neurology, Neurosurgery & ; Psychiatry 80, n^o 9 (29 mars 2009) : 998–1001. http://dx.doi.org/10.1136/jnnp.2008.171496.

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Yousefzadeh-Nowshahr, Elham, Gordon Winter, Peter Bohn, Katharina Kneer, Christine A. F. von Arnim, Markus Otto, Christoph Solbach et al. « Quantitative analysis of regional distribution of tau pathology with 11C-PBB3-PET in a clinical setting ». PLOS ONE 17, n^o 4 (11 avril 2022) : e0266906. http://dx.doi.org/10.1371/journal.pone.0266906.

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Purpose The recent developments of tau-positron emission tomography (tau-PET) enable in vivo assessment of neuropathological tau aggregates. Among the tau-specific tracers, the application of 11C-pyridinyl-butadienyl-benzothiazole 3 (11C-PBB3) in PET shows high sensitivity to Alzheimer disease (AD)-related tau deposition. The current study investigates the regional tau load in patients within the AD continuum, biomarker-negative individuals (BN) and patients with suspected non-AD pathophysiology (SNAP) using 11C-PBB3-PET. Materials and methods A total of 23 memory clinic outpatients with recent decline of episodic memory were examined using 11C-PBB3-PET. Pittsburg compound B (11C-PIB) PET was available for 17, 18F-flurodeoxyglucose (18F-FDG) PET for 16, and cerebrospinal fluid (CSF) protein levels for 11 patients. CSF biomarkers were considered abnormal based on Aβ42 (< 600 ng/L) and t-tau (> 450 ng/L). The PET biomarkers were classified as positive or negative using statistical parametric mapping (SPM) analysis and visual assessment. Using the amyloid/tau/neurodegeneration (A/T/N) scheme, patients were grouped as within the AD continuum, SNAP, and BN based on amyloid and neurodegeneration status. The 11C-PBB3 load detected by PET was compared among the groups using both atlas-based and voxel-wise analyses. Results Seven patients were identified as within the AD continuum, 10 SNAP and 6 BN. In voxel-wise analysis, significantly higher 11C-PBB3 binding was observed in the AD continuum group compared to the BN patients in the cingulate gyrus, tempo-parieto-occipital junction and frontal lobe. Compared to the SNAP group, patients within the AD continuum had a considerably increased 11C-PBB3 uptake in the posterior cingulate cortex. There was no significant difference between SNAP and BN groups. The atlas-based analysis supported the outcome of the voxel-wise quantification analysis. Conclusion Our results suggest that 11C-PBB3-PET can effectively analyze regional tau load and has the potential to differentiate patients in the AD continuum group from the BN and SNAP group.

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Wang, Yue, Fanghua Lou, Yonggang Li, Fang Liu, Ying Wang, Li Cai, Marc L. Gordon, Yuanyuan Zhang et Nan Zhang. « Clinical, Neuropsychological, and Neuroimaging Characteristics of Amyloid- positive vs. Amyloid-negative Patients with Clinically Diagnosed Alzheimer’s Disease and Amnestic Mild Cognitive Impairment ». Current Alzheimer Research 18, n^o 6 (mai 2021) : 523–32. http://dx.doi.org/10.2174/1567205018666211001113349.

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Background: A significant proportion of patients with clinically diagnosed Alzheimer’s Disease (AD) and an even higher proportion of patients with amnestic mild cognitive impairment (aMCI) do not show evidence of amyloid deposition on Positron Emission Tomography (PET) with amyloid-binding tracers such as 11C-labeled Pittsburgh Compound B (PiB). Objective: This study aimed to identify clinical, neuropsychological and neuroimaging factors that might suggest amyloid neuropathology in patients with clinically suspected AD or aMCI. Methods: Forty patients with mild to moderate AD and 23 patients with aMCI who were clinically diagnosed in our memory clinic and had PiB PET scans were included. Clinical, neuropsychological, and imaging characteristics, such as Medial Temporal lobe Atrophy (MTA) and White Matter Hyperintensities (WMH) on MRI and metabolic pattern on 18F-labeled fluorodeoxyglucose (FDG) PET, were compared between patients with PiB positive and negative PET results for AD, aMCI, and all subjects combined, respectively. Results: Compared with PiB positive patients, PiB negative patients had a higher prevalence of hypertension history, better performance on the Mini-Mental State Examination, the Rey Auditory Verbal Learning Test, and the Judgement of Line Orientation, lower score of MTA, and were less likely to have temporoparietal-predominant hypometabolism on FDG PET. Affective symptoms were less common in PiB negative patients diagnosed with AD, and the Animal Fluency Test score was higher in PiB negative patients diagnosed with aMCI. Conclusion: In patients with clinically diagnosed AD or aMCI, absence of a history of hypertension, deficits in verbal learning and memory, visuospatial function, semantic verbal fluency, presence of affective symptoms, MTA on MRI, and temporoparietal hypometabolism on FDG PET suggested amyloid deposition in the brain.

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Betthauser, Tobey J., Rebecca L. Koscik, Erin M. Jonaitis, Samantha L. Allison, Karly A. Cody, Claire M. Erickson, Howard A. Rowley et al. « Amyloid and tau imaging biomarkers explain cognitive decline from late middle-age ». Brain 143, n^o 1 (27 décembre 2019) : 320–35. http://dx.doi.org/10.1093/brain/awz378.

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Abstract This study investigated differences in retrospective cognitive trajectories between amyloid and tau PET biomarker stratified groups in initially cognitively unimpaired participants sampled from the Wisconsin Registry for Alzheimer’s Prevention. One hundred and sixty-seven initially unimpaired individuals (baseline age 59 ± 6 years; 115 females) were stratified by elevated amyloid-β and tau status based on 11C-Pittsburgh compound B (PiB) and 18F-MK-6240 PET imaging. Mixed effects models were used to determine if longitudinal cognitive trajectories based on a composite of cognitive tests including memory and executive function differed between biomarker groups. Secondary analyses investigated group differences for a variety of cross-sectional health and cognitive tests, and associations between 18F-MK-6240, 11C-PiB, and age. A significant group × age interaction was observed with post hoc comparisons indicating that the group with both elevated amyloid and tau pathophysiology were declining approximately three times faster in retrospective cognition compared to those with just one or no elevated biomarkers. This result was robust against various thresholds and medial temporal lobe regions defining elevated tau. Participants were relatively healthy and mostly did not differ between biomarker groups in health factors at the beginning or end of study, or most cognitive measures at study entry. Analyses investigating association between age, MK-6240 and PiB indicated weak associations between age and 18F-MK-6240 in tangle-associated regions, which were negligible after adjusting for 11C-PiB. Strong associations, particularly in entorhinal cortex, hippocampus and amygdala, were observed between 18F-MK-6240 and global 11C-PiB in regions associated with Braak neurofibrillary tangle stages I–VI. These results suggest that the combination of pathological amyloid and tau is detrimental to cognitive decline in preclinical Alzheimer’s disease during late middle-age. Within the Alzheimer’s disease continuum, middle-age health factors likely do not greatly influence preclinical cognitive decline. Future studies in a larger preclinical sample are needed to determine if and to what extent individual contributions of amyloid and tau affect cognitive decline. 18F-MK-6240 shows promise as a sensitive biomarker for detecting neurofibrillary tangles in preclinical Alzheimer’s disease.

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Kitamura, Soichiro, Hitoshi Shimada, Fumitoshi Niwa, Hironobu Endo, Hitoshi Shinotoh, Keisuke Takahata, Manabu Kubota et al. « Tau-induced focal neurotoxicity and network disruption related to apathy in Alzheimer’s disease ». Journal of Neurology, Neurosurgery & ; Psychiatry 89, n^o 11 (8 juin 2018) : 1208–14. http://dx.doi.org/10.1136/jnnp-2018-317970.

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ObjectiveApathy is a common neuropsychological symptom in Alzheimer’s disease (AD), and previous studies demonstrated that neuronal loss and network disruption in some brain regions play pivotal roles in the pathogenesis of apathy. However, contributions of tau and amyloid-β (Aβ) depositions, pathological hallmarks of AD, to the manifestation of apathy remain elusive.MethodsSeventeen patients with AD underwent positron emission tomography (PET) with11C-pyridinyl-butadienyl-benzothiazole 3 (11C-PBB3) and11C-Pittsburgh compound-B (11C-PiB) to estimate tau and Aβ accumulations using standardised uptake value ratio (SUVR) images.11C-PBB3 and11C-PiB SUVR were compared between AD patients with high and low Apathy Scale (AS) scores. Additionally, volumetric and diffusion tensor MRI was performed in those areas where any significant difference was observed in PET analyses. Correlation and path analyses among AS and estimated imaging parameters were also conducted.ResultsAD patients with high AS scores showed higher11C-PBB3 SUVR in the orbitofrontal cortex (OFC) than those with low AS scores, while11C-PiB SUVR in any brain regions did not differ between them. Elevated11C-PBB3 SUVR in OFC, decreased OFC thickness and decreased fractional anisotropy (FA) in the uncinate fasciculus (UNC), which is structurally connected to OFC, correlated significantly with increased scores of the AS. Path analysis indicated that increased11C-PBB3 SUVR in OFC affects apathy directly and through reduction of OFC thickness and subsequent decrease of FA in UNC.ConclusionsThe present findings suggested that tau pathology in OFC may provoke focal neurotoxicity in OFC and the following disruption of the OFC-UNC network, leading to the emergence and progression of apathy in AD.

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Bilgel, Murat, Lori Beason-Held, Yang An, Yun Zhou, Dean F. Wong et Susan M. Resnick. « Longitudinal evaluation of surrogates of regional cerebral blood flow computed from dynamic amyloid PET imaging ». Journal of Cerebral Blood Flow & ; Metabolism 40, n^o 2 (12 février 2019) : 288–97. http://dx.doi.org/10.1177/0271678x19830537.

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Surrogates of neuronal activity, typically measured by regional cerebral blood flow (rCBF) or glucose metabolism, can be estimated from dynamic amyloid PET imaging. Using data for 149 participants (345 visits) from the Baltimore Longitudinal Study of Aging, we assessed whether the average of early amyloid frames (EA) and R1 computed from dynamic 11C-Pittsburgh compound B (PiB) PET can serve as surrogates of rCBF computed from 15O-H2O-PET. R1 had the highest longitudinal test–retest reliability. Interquartile range (IQR) of cross-sectional Pearson correlations with rCBF was 0.60–0.72 for EA and 0.63–0.72 for R1. Correlations between rates of change were lower (IQR 0.22–0.50 for EA, 0.25–0.55 for R1). Values in the Alzheimer’s metabolic signature meta-ROI were negatively associated with age and exhibited longitudinal declines for each PET measure. In age-adjusted analyses, meta-ROI rCBF and R1 were lower among amyloid+ individuals; EA and R1 were lower among males. Regional PiB-based measures, in particular R1, can be suitable surrogates of rCBF. Dynamic PiB-PET may obviate the need for a separate scan to measure neuronal activity, thereby reducing patient burden, radioactivity exposure, and cost.

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Chen, Y. J., B. L. Rosario, W. Mowrey, C. M. Laymon, X. Lu, O. L. Lopez, W. E. Klunk, B. J. Lopresti, C. A. Mathis et J. C. Price. « Relative 11C-PiB Delivery as a Proxy of Relative CBF : Quantitative Evaluation Using Single-Session 15O-Water and 11C-PiB PET ». Journal of Nuclear Medicine 56, n^o 8 (4 juin 2015) : 1199–205. http://dx.doi.org/10.2967/jnumed.114.152405.

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Kim, Chi Hun, Sang Won Seo, Geon Ha Kim, Ji Soo Shin, Hanna Cho, Young Noh, Suk-Hui Kim et al. « Cortical Thinning in Subcortical Vascular Dementia with Negative 11C-PiB PET ». Journal of Alzheimer's Disease 31, n^o 2 (31 juillet 2012) : 315–23. http://dx.doi.org/10.3233/jad-2012-111832.

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Sengoku, Renpei, Satoshi Matsushima, Yoshitake Murakami, Takahiro Fukuda, Aya M. Tokumaru, Masaya Hashimoto, Masahiko Suzuki, Kiichi Ishiwata, Kenji Ishii et Soichiro Mochio. « 11C-PiB PET Imaging of Encephalopathy Associated with Cerebral Amyloid Angiopathy ». Internal Medicine 53, n^o 17 (2014) : 1997–2000. http://dx.doi.org/10.2169/internalmedicine.53.1731.

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Zhou, Luping, Olivier Salvado, Vincent Dore, Pierrick Bourgeat, Parnesh Raniga, S. Lance Macaulay, David Ames et al. « MR-Less Surface-Based Amyloid Assessment Based on 11C PiB PET ». PLoS ONE 9, n^o 1 (10 janvier 2014) : e84777. http://dx.doi.org/10.1371/journal.pone.0084777.

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Fripp, Jurgen, Pierrick Bourgeat, Oscar Acosta, Parnesh Raniga, Sebastien Ourselin, Collin Masters, David Ames et al. « P1-160 : Modeling the appearance variation of 11c Pib PET-images ». Alzheimer's & ; Dementia 4 (juillet 2008) : T254. http://dx.doi.org/10.1016/j.jalz.2008.05.748.

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Rabinovici, G. D., A. J. Furst, J. P. O'Neil, C. A. Racine, E. C. Mormino, S. L. Baker, S. Chetty et al. « 11C-PIB PET imaging in Alzheimer disease and frontotemporal lobar degeneration ». Neurology 68, n^o 15 (9 avril 2007) : 1205–12. http://dx.doi.org/10.1212/01.wnl.0000259035.98480.ed.

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Chaves, Hernan, Yanina Bergamo, Santiago Paz, Flavio Sanchez et Silvia Vazquez. « Sphenoid Wing Meningioma Behavior on 11C-PiB and 18F-FDG PET ». Clinical Nuclear Medicine 40, n^o 1 (janvier 2015) : e81-e82. http://dx.doi.org/10.1097/rlu.0000000000000407.

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Ishimura, Mariko, Yuka Yamamoto, Naruhide Kimura, Hiroshi Hoshikawa et Yoshihiro Nishiyama. « 11C-PiB PET/CT in Nasopharyngeal Amyloidosis Associated with Multiple Myeloma ». Clinical Nuclear Medicine 40, n^o 2 (février 2015) : e161-e162. http://dx.doi.org/10.1097/rlu.0000000000000558.

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Suotunen, Timo, Jussi Hirvonen, Pirjo Immonen-Räihä, Sargo Aalto, Irina Lisinen, Eveliina Arponen, Mika Teräs et al. « Visual assessment of [11C]PIB PET in patients with cognitive impairment ». European Journal of Nuclear Medicine and Molecular Imaging 37, n^o 6 (9 février 2010) : 1141–47. http://dx.doi.org/10.1007/s00259-010-1382-8.

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Ikonomovic, Milos D., Christopher J. Buckley, Eric E. Abrahamson, Julia K. Kofler, Chester A. Mathis, William E. Klunk et Gill Farrar. « Post-mortem analyses of PiB and flutemetamol in diffuse and cored amyloid-β plaques in Alzheimer’s disease ». Acta Neuropathologica 140, n^o 4 (9 août 2020) : 463–76. http://dx.doi.org/10.1007/s00401-020-02175-1.

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Abstract Specificity and sensitivity of positron emission tomography (PET) radiopharmaceuticals targeting fibrillar amyloid-β (Aβ) deposits is high for detection of neuritic Aβ plaques, a mature form of Aβ deposits which often have dense Aβ core (i.e., cored plaques). However, imaging-to-autopsy validation studies of amyloid PET radioligands have identified several false positive cases all of which had mainly diffuse Aβ plaques (i.e., plaques without neuritic pathology or dense amyloid core), and high amyloid PET signal was reported in the striatum where diffuse plaques predominate in Alzheimer’s disease (AD). Relative contributions of different plaque types to amyloid PET signal is unclear, particularly in neocortical areas where they are intermixed in AD. In vitro binding assay and autoradiography were performed using [3H]flutemetamol and [3H]Pittsburgh Compound-B (PiB) in frozen brain homogenates from 30 autopsy cases including sporadic AD and non-AD controls with a range of brain Aβ burden and plaque density. Fixed tissue sections of frontal cortex and caudate from 10 of the AD cases were processed for microscopy using fluorescent derivatives of flutemetamol (cyano-flutemetamol) and PiB (cyano-PiB) and compared to Aβ immunohistochemistry and pan-amyloid (X-34) histology. Using epifluorescence microscopy, percent area coverage and fluorescence output values of cyano-PiB- and cyano-flutemetamol-labeled plaques in two-dimensional microscopic fields were then calculated and combined to obtain integrated density measurements. Using confocal microscopy, we analysed total fluorescence output of the entire three-dimensional volume of individual cored plaques and diffuse plaques labeled with cyano-flutemetamol or cyano-PiB. [3H]Flutemetamol and [3H]PiB binding values in tissue homogenates correlated strongly and their binding pattern in tissue sections, as seen on autoradiograms, overlapped the pattern of Aβ-immunoreactive plaques on directly adjacent sections. Cyano-flutemetamol and cyano-PiB fluorescence was prominent in cored plaques and less so in diffuse plaques. Across brain regions and cases, percent area coverage of cyano-flutemetamol-labeled plaques correlated strongly with cyano-PiB-labeled and Aβ-immunoreactive plaques. For both ligands, plaque burden, calculated as percent area coverage of all Aβ plaque types, was similar in frontal cortex and caudate regions, while integrated density values were significantly greater in frontal cortex, which contained both cored plaques and diffuse plaques, compared to the caudate, which contained only diffuse plaques. Three-dimensional analysis of individual plaques labeled with either ligand showed that total fluorescence output of a single cored plaque was equivalent to total fluorescence output of approximately three diffuse plaques of similar volume. Our results indicate that [18F]flutemetamol and [11C]PiB PET signal is influenced by both diffuse plaques and cored plaques, and therefore is likely a function of plaque size and density of Aβ fibrils in plaques. Brain areas with large volumes/frequencies of diffuse plaques could yield [18F]flutemetamol and [11C]PiB PET retention levels comparable to brain regions with a lower volume/frequency of cored plaques.

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Shi, Zhihong, Ying Wang, Shuai Liu, Mengyuan Liu, Shuling Liu, Yuying Zhou, Jinhuan Wang et al. « Clinical and Neuroimaging Characterization of Chinese Dementia Patients with PSEN1 and PSEN2 Mutations ». Dementia and Geriatric Cognitive Disorders 39, n^o 1-2 (15 octobre 2014) : 32–40. http://dx.doi.org/10.1159/000366272.

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Background: Alzheimer's disease (AD) and frontotemporal dementia (FTD) are two common forms of primary neurodegenerative dementia. Mutations in 3 genes (PSEN1, PSEN2, and APP) have been identified in patients with early-onset AD. Methods: We performed gene sequencing in PSEN1, PSEN2, and APP in 61 AD and 35 FTD Chinese patients. Amyloid load using 11C-labeled Pittsburgh compound B (11C-PIB) positron emission tomography (PET) and cerebral glucose metabolism using 18F-fludeoxyglucose PET were evaluated in patients carrying mutations. Results: We identified 1 known pathogenic PSEN1 (p.His163Arg, c.488A>G) mutation and 3 novel PSEN2 mutations in 6 patients. The novel mutation PSEN2 (p.His169Asn, c.505C>A) was identified in 1 patient with familial late-onset AD and in 1 sporadic FTD patient. The PSEN2 (p.Val214Leu, c.640G>T; p.Lys82Arg, c.245A>G) mutations were identified in 2 early-onset AD patients and 1 early-onset AD patient, respectively. Three patients with PSEN2 mutations were observed to have PIB retention on the cortex and striatum. One patient with the FTD phenotype was not observed to have PIB retention. Conclusion: PSEN2 mutations are common in the Chinese Han population with a history of AD and FTD. Pathogenic mutations or risk variants in the PSEN2 gene can influence both FTD and AD phenotypic traits and show variations in neuroimaging characterization. © 2014 S. Karger AG, Basel

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Kantarci, Kejal, Val J. Lowe, Qin Chen, Scott A. Przybelski, Timothy G. Lesnick, Christopher G. Schwarz, Matthew L. Senjem et al. « β-Amyloid PET and neuropathology in dementia with Lewy bodies ». Neurology 94, n^o 3 (20 décembre 2019) : e282-e291. http://dx.doi.org/10.1212/wnl.0000000000008818.

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Objectiveβ-Amyloid (Aβ) pathology is common in patients with probable dementia with Lewy bodies (DLB). However, the pathologic basis and the differential diagnostic performance of Aβ PET are not established in DLB. Our objective was to investigate the pathologic correlates of 11C-Pittsburgh compound B(PiB) uptake on PET in cases with antemortem diagnosis of probable DLB or Lewy body disease (LBD) at autopsy.MethodsAutopsied cases who underwent antemortem PiB-PET and were assigned a clinical diagnosis of probable DLB or LBD at autopsy were included (n = 39). The primary endpoint was pathologic diagnosis of LBD, Alzheimer disease (AD), or mixed (LBD and AD) pathology; the secondary endpoints included Thal Aβ phase and diffuse and neuritic Aβ plaques.ResultsLower global cortical PiB standardized uptake value ratio (SUVr) distinguished cases with LBD from cases with AD or mixed pathology with an accuracy of 93%. Greater global cortical PiB SUVr correlated with higher Thal Aβ phase (r = 0.75, p ≤ 0.001). Voxel–based analysis demonstrated that Aβ pathology relatively spared the occipital lobes in cases with mixed pathology and LBD compared to cases with AD without LBD, in whom the entire cerebral cortex was involved. Global cortical PiB SUVr was associated primarily with the abundance of diffuse Aβ plaques in cases with LBD in a multivariable regression model.ConclusionLower PiB uptake accurately distinguishes cases with LBD from cases with AD or mixed pathology, correlating with the Thal Aβ phase. The severity of diffuse Aβ pathology is the primary contributor to elevated PiB uptake in LBD.Classification of evidenceThis study provides Class III evidence that lower PiB uptake accurately distinguishes patients with LBD from those with AD or mixed pathology.

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Képes, Zita, Alexandra Barkóczi, Judit P. Szabó, Ibolya Kálmán-Szabó, Viktória Arató, István Jószai, Ádám Deák, István Kertész, István Hajdu et György Trencsényi. « In Vivo Preclinical Assessment of β-Amyloid–Affine [11C]C-PIB Accumulation in Aluminium-Induced Alzheimer’s Disease-Resembling Hypercholesterinaemic Rat Model ». International Journal of Molecular Sciences 23, n^o 22 (12 novembre 2022) : 13950. http://dx.doi.org/10.3390/ijms232213950.

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Aluminum (Al) excess and hypercholesterinaemia are established risks of Alzheimer’s disease (AD). The aim of this study was to establish an AD-resembling hypercholesterinaemic animal model—with the involvement of 8 week and 48 week-old Fischer-344 rats—by Al administration for the safe and rapid verification of β-amyloid-targeted positron emission tomography (PET) radiopharmaceuticals. Measurement of lipid parameters and β-amyloid–affine [11C]C-Pittsburgh Compound B ([11C]C-PIB) PET examinations were performed. Compared with the control, the significantly elevated cholesterol and LDL levels of the rats receiving the cholesterol-rich diet support the development of hypercholesterinaemia (p ≤ 0.01). In the older cohort, a notably increased age-related radiopharmaceutical accumulation was registered compared to in the young (p ≤ 0.05; p ≤ 0.01). A monotherapy-induced slight elevation of mean standardised uptake values (SUVmean) was statistically not significant; however, adult rats administered a combined diet expressed remarkable SUVmean increment compared to the adult control (SUVmean: from 0.78 ± 0.16 to 1.99 ± 0.28). One and two months after restoration to normal diet, the cerebral [11C]C-PIB accumulation of AD-mimicking animals decreased by half and a third, respectively, to the baseline value. The proposed in vivo Al-induced AD-resembling animal system seems to be adequate for the understanding of AD neuropathology and future drug testing and radiopharmaceutical development.

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Knopman, David S., Emily S. Lundt, Terry M. Therneau, Prashanthi Vemuri, Val J. Lowe, Kejal Kantarci, Jeffrey L. Gunter et al. « Entorhinal cortex tau, amyloid-β, cortical thickness and memory performance in non-demented subjects ». Brain 142, n^o 4 (12 février 2019) : 1148–60. http://dx.doi.org/10.1093/brain/awz025.

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AbstractAs more biomarkers for Alzheimer’s disease and age-related brain conditions become available, more sophisticated analytic approaches are needed to take full advantage of the information they convey. Most work has been done using categorical approaches but the joint relationships of tau PET, amyloid PET and cortical thickness in their continuous distributions to cognition have been under-explored. We evaluated non-demented subjects over age 50 years in the Mayo Clinic Study of Aging, 2037 of whom had undergone 3 T MRI scan, 985 amyloid PET scan with 11C-Pittsburgh compound B (PIB) and MRI, and 577 PIB-PET, 18F-AV1451 flortaucipir PET and MRI. Participants received a nine-test cognitive battery. Three test scores (logical memory delayed recall, visual reproduction delayed recall and auditory verbal learning test delayed recall) were used to generate a memory composite z-score. We used Gradient Boosting Machine models to analyse the relationship between regional cortical thickness, flortaucipir PET signal, PIB-PET signal and memory z-scores. Age, education, sex and number of test exposures were included in the model as covariates. In this population-based study of non-demented subjects, most of the associations between biomarkers and memory z-scores accrued after 70 years of age. Entorhinal cortex exhibited the strongest associations between biomarkers and memory z-scores. Other temporal regions showed similar but attenuated associations, and non-temporal regions had negligible associations between memory z-scores and biomarkers. Entorhinal flortaucipir PET signal, PIB-PET signal and entorhinal cortical thickness were independently and additively associated with declining memory z-scores. In contrast to global PIB-PET signal where only very high amyloid-β levels were associated low memory z-scores, entorhinal flortaucipir PET signal just above background levels was associated with low memory z-scores. The lowest memory z-scores occurred with the confluence of elevated entorhinal flortaucipir PET signal and lower entorhinal cortical thickness.

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