<?xml version="1.0" encoding="UTF-8" ?><xml><records><record><database name="neumaier.enl" path="C:\Users\b.mayer\Desktop\UKZ Bilder\neumaier.enl">neumaier.enl</database><source-app name="EndNote" version="21.4">EndNote</source-app><rec-number>1</rec-number><foreign-keys><key app="EN" db-id="avvwwzara0ssdaef0vjv92r1wtp5sxstv2vz">1</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Craig, Austin</style></author><author><style face="normal" font="default" size="100%">Kolks, Niklas</style></author><author><style face="normal" font="default" size="100%">Urusova, Elizaveta A.</style></author><author><style face="normal" font="default" size="100%">Zischler, Johannes</style></author><author><style face="normal" font="default" size="100%">Brugger, Melanie</style></author><author><style face="normal" font="default" size="100%">Endepols, Heike</style></author><author><style face="normal" font="default" size="100%">Neumaier, Bernd</style></author><author><style face="normal" font="default" size="100%">Zlatopolskiy, Boris D.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Preparation of labeled aromatic amino acids via late-stage 18F-fluorination of chiral nickel and copper complexes</style></title><secondary-title><style face="normal" font="default" size="100%">Chemical Communications</style></secondary-title></titles><periodical><full-title><style face="normal" font="default" size="100%">Chemical Communications</style></full-title></periodical><pages><style face="normal" font="default" size="100%">9505-9508</style></pages><volume><style face="normal" font="default" size="100%">56</style></volume><number><style face="normal" font="default" size="100%">66</style></number><dates><year><style face="normal" font="default" size="100%">2020</style></year></dates><publisher><style face="normal" font="default" size="100%">The Royal Society of Chemistry</style></publisher><isbn><style face="normal" font="default" size="100%">1359-7345</style></isbn><abstract><style face="normal" font="default" size="100%">A general protocol for the preparation of 18F-labeled AAAs and α-methyl-AAAs applying alcohol-enhanced Cu-mediated radiofluorination of Bpin-substituted chiral complexes using Ni/Cu-BPX templates as double protecting groups is reported. The chiral auxiliaries are easily accessible from commercially available starting materials in a few synthetic steps. The versatility of the method was demonstrated by the high-yielding preparation of a series of [18F]F-AAAs and the successful implementation of the protocol into automated radiosynthesis modules.</style></abstract><work-type><style face="normal" font="default" size="100%">10.1039/D0CC02223C</style></work-type><urls><related-urls><url><style face="normal" font="default" size="100%">http://dx.doi.org/10.1039/D0CC02223C</style></url></related-urls></urls><electronic-resource-num><style face="normal" font="default" size="100%">10.1039/D0CC02223C</style></electronic-resource-num></record><record><database name="neumaier.enl" path="C:\Users\b.mayer\Desktop\UKZ Bilder\neumaier.enl">neumaier.enl</database><source-app name="EndNote" version="21.4">EndNote</source-app><rec-number>2</rec-number><foreign-keys><key app="EN" db-id="avvwwzara0ssdaef0vjv92r1wtp5sxstv2vz">2</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Dronse, Julian</style></author><author><style face="normal" font="default" size="100%">Fliessbach, Klaus</style></author><author><style face="normal" font="default" size="100%">Bischof, Gérard N.</style></author><author><style face="normal" font="default" size="100%">von Reutern, Boris</style></author><author><style face="normal" font="default" size="100%">Faber, Jennifer</style></author><author><style face="normal" font="default" size="100%">Hammes, Jochen</style></author><author><style face="normal" font="default" size="100%">Kuhnert, Georg</style></author><author><style face="normal" font="default" size="100%">Neumaier, Bernd</style></author><author><style face="normal" font="default" size="100%">Onur, Oezguer A.</style></author><author><style face="normal" font="default" size="100%">Kukolja, Juraj</style></author><author><style face="normal" font="default" size="100%">van Eimeren, Thilo</style></author><author><style face="normal" font="default" size="100%">Jessen, Frank</style></author><author><style face="normal" font="default" size="100%">Fink, Gereon R.</style></author><author><style face="normal" font="default" size="100%">Klockgether, Thomas</style></author><author><style face="normal" font="default" size="100%">Drzezga, Alexander</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">In vivo Patterns of Tau Pathology, Amyloid-β Burden, and Neuronal Dysfunction in Clinical Variants of Alzheimer’s Disease</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of Alzheimer&apos;s Disease</style></secondary-title></titles><periodical><full-title><style face="normal" font="default" size="100%">Journal of Alzheimer&apos;s Disease</style></full-title></periodical><pages><style face="normal" font="default" size="100%">465-471</style></pages><volume><style face="normal" font="default" size="100%">55</style></volume><keywords><keyword><style face="normal" font="default" size="100%">Alzheimer’s disease</style></keyword><keyword><style face="normal" font="default" size="100%">amyloid</style></keyword><keyword><style face="normal" font="default" size="100%">18F-AV-1451</style></keyword><keyword><style face="normal" font="default" size="100%">18F-FDG</style></keyword><keyword><style face="normal" font="default" size="100%">molecular imaging</style></keyword><keyword><style face="normal" font="default" size="100%">multimodal imaging</style></keyword><keyword><style face="normal" font="default" size="100%">Pittsburghcompound B</style></keyword><keyword><style face="normal" font="default" size="100%">positron-emission tomography</style></keyword><keyword><style face="normal" font="default" size="100%">T-807</style></keyword><keyword><style face="normal" font="default" size="100%">tau protein</style></keyword></keywords><dates><year><style face="normal" font="default" size="100%">2017</style></year></dates><publisher><style face="normal" font="default" size="100%">IOS Press</style></publisher><isbn><style face="normal" font="default" size="100%">1875-8908</style></isbn><abstract><style face="normal" font="default" size="100%">The clinical heterogeneity of Alzheimer’s disease is not reflected in the rather diffuse cortical deposition of amyloid-β. We assessed the relationship between clinical symptoms, in vivo tau pathology, amyloid distribution, and hypometabolism in variants of Alzheimer’s disease using novel multimodal PET imaging techniques. Tau pathology was primarily observed in brain regions related to clinical symptoms and overlapped with areas of hypometabolism. In contrast, amyloid-β deposition was diffusely distributed over the entire cortex. Tau PET imaging may thus serve as a valuable biomarker for the localization of neuronal injury in vivo and may help to validate atypical subtypes of Alzheimer’s disease.</style></abstract><urls></urls><electronic-resource-num><style face="normal" font="default" size="100%">10.3233/JAD-160316</style></electronic-resource-num></record><record><database name="neumaier.enl" path="C:\Users\b.mayer\Desktop\UKZ Bilder\neumaier.enl">neumaier.enl</database><source-app name="EndNote" version="21.4">EndNote</source-app><rec-number>11</rec-number><foreign-keys><key app="EN" db-id="avvwwzara0ssdaef0vjv92r1wtp5sxstv2vz">11</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Gossen, J.</style></author><author><style face="normal" font="default" size="100%">Ribeiro, R. P.</style></author><author><style face="normal" font="default" size="100%">Bier, D.</style></author><author><style face="normal" font="default" size="100%">Neumaier, B.</style></author><author><style face="normal" font="default" size="100%">Carloni, P.</style></author><author><style face="normal" font="default" size="100%">Giorgetti, A.</style></author><author><style face="normal" font="default" size="100%">Rossetti, G.</style></author></authors></contributors><auth-address><style face="normal" font="default" size="100%">Institute for Computational Biomedicine (INM-9/IAS-5) Forschungszentrum Julich Wilhelm-Johnen-Strasse 52428 Julich Germany g.rossetti@fz-juelich.de.&#xD;Faculty of Mathematics, Computer Science and Natural Sciences RWTH Aachen University Aachen Germany.&#xD;Institute of Neuroscience and Medicine, Nuclear Chemistry (INM-5), Forschungszentrum Julich GmbH Wilhelm-Johnen-Strasse 52428 Julich Germany.&#xD;Institute of Radiochemistry and Experimental Molecular Imaging, University of Cologne, Faculty of Medicine and University Hospital Cologne Kerpener Strasse 62 50937 Cologne Germany.&#xD;JARA-Institut Molecular Neuroscience and Neuroimaging (INM-11) Forschungszentrum Julich Wilhelm-Johnen-Strasse 52428 Julich Germany.&#xD;Department of Biotechnology University of Verona Verona Italy.&#xD;Julich Supercomputing Centre (JSC) Forschungszentrum Julich Julich Germany.&#xD;Department of Neurology University Hospital Aachen (UKA), RWTH Aachen University Aachen Germany.</style></auth-address><titles><title><style face="normal" font="default" size="100%">AI-based identification of therapeutic agents targeting GPCRs: introducing ligand type classifiers and systems biology</style></title><secondary-title><style face="normal" font="default" size="100%">Chem Sci</style></secondary-title></titles><periodical><full-title><style face="normal" font="default" size="100%">Chem Sci</style></full-title></periodical><pages><style face="normal" font="default" size="100%">8651-8661</style></pages><volume><style face="normal" font="default" size="100%">14</style></volume><number><style face="normal" font="default" size="100%">32</style></number><edition><style face="normal" font="default" size="100%">20230724</style></edition><dates><year><style face="normal" font="default" size="100%">2023</style></year><pub-dates><date><style face="normal" font="default" size="100%">Aug 16</style></date></pub-dates></dates><isbn><style face="normal" font="default" size="100%">2041-6520 (Print)&#xD;2041-6539 (Electronic)&#xD;2041-6520 (Linking)</style></isbn><accession-num><style face="normal" font="default" size="100%">37592985</style></accession-num><abstract><style face="normal" font="default" size="100%">Identifying ligands targeting G protein coupled receptors (GPCRs) with novel chemotypes other than the physiological ligands is a challenge for in silico screening campaigns. Here we present an approach that identifies novel chemotype ligands by combining structural data with a random forest agonist/antagonist classifier and a signal-transduction kinetic model. As a test case, we apply this approach to identify novel antagonists of the human adenosine transmembrane receptor type 2A, an attractive target against Parkinson&apos;s disease and cancer. The identified antagonists were tested here in a radio ligand binding assay. Among those, we found a promising ligand whose chemotype differs significantly from all so-far reported antagonists, with a binding affinity of 310 +/- 23.4 nM. Thus, our protocol emerges as a powerful approach to identify promising ligand candidates with novel chemotypes while preserving antagonistic potential and affinity in the nanomolar range.</style></abstract><notes><style face="normal" font="default" size="100%">Gossen, Jonas&#xD;Ribeiro, Rui Pedro&#xD;Bier, Dirk&#xD;Neumaier, Bernd&#xD;Carloni, Paolo&#xD;Giorgetti, Alejandro&#xD;Rossetti, Giulia&#xD;eng&#xD;England&#xD;2023/08/18&#xD;Chem Sci. 2023 Jul 24;14(32):8651-8661. doi: 10.1039/d3sc02352d. eCollection 2023 Aug 16.</style></notes><urls><related-urls><url><style face="normal" font="default" size="100%">https://www.ncbi.nlm.nih.gov/pubmed/37592985</style></url></related-urls></urls><custom1><style face="normal" font="default" size="100%">The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.</style></custom1><custom2><style face="normal" font="default" size="100%">PMC10430665</style></custom2><electronic-resource-num><style face="normal" font="default" size="100%">10.1039/d3sc02352d</style></electronic-resource-num><remote-database-name><style face="normal" font="default" size="100%">PubMed-not-MEDLINE</style></remote-database-name><remote-database-provider><style face="normal" font="default" size="100%">NLM</style></remote-database-provider></record><record><database name="neumaier.enl" path="C:\Users\b.mayer\Desktop\UKZ Bilder\neumaier.enl">neumaier.enl</database><source-app name="EndNote" version="21.4">EndNote</source-app><rec-number>3</rec-number><foreign-keys><key app="EN" db-id="avvwwzara0ssdaef0vjv92r1wtp5sxstv2vz">3</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Hoenig, Merle C.</style></author><author><style face="normal" font="default" size="100%">Bischof, Gérard N.</style></author><author><style face="normal" font="default" size="100%">Seemiller, Joseph</style></author><author><style face="normal" font="default" size="100%">Hammes, Jochen</style></author><author><style face="normal" font="default" size="100%">Kukolja, Juraj</style></author><author><style face="normal" font="default" size="100%">Onur, Özgür A.</style></author><author><style face="normal" font="default" size="100%">Jessen, Frank</style></author><author><style face="normal" font="default" size="100%">Fliessbach, Klaus</style></author><author><style face="normal" font="default" size="100%">Neumaier, Bernd</style></author><author><style face="normal" font="default" size="100%">Fink, Gereon R.</style></author><author><style face="normal" font="default" size="100%">van Eimeren, Thilo</style></author><author><style face="normal" font="default" size="100%">Drzezga, Alexander</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Networks of tau distribution in Alzheimer’s disease</style></title><secondary-title><style face="normal" font="default" size="100%">Brain</style></secondary-title></titles><periodical><full-title><style face="normal" font="default" size="100%">Brain</style></full-title></periodical><pages><style face="normal" font="default" size="100%">568-581</style></pages><volume><style face="normal" font="default" size="100%">141</style></volume><number><style face="normal" font="default" size="100%">2</style></number><dates><year><style face="normal" font="default" size="100%">2018</style></year></dates><isbn><style face="normal" font="default" size="100%">0006-8950</style></isbn><abstract><style face="normal" font="default" size="100%">See Whitwell (doi:10.1093/brain/awy001) for a scientific commentary on this article.A stereotypical anatomical propagation of tau pathology has been described in Alzheimer’s disease. According to recent concepts (network degeneration hypothesis), this propagation is thought to be indicative of misfolded tau proteins possibly spreading along functional networks. If true, tau pathology accumulation should correlate in functionally connected brain regions. Therefore, we examined whether independent components could be identified in the distribution pattern of in vivo tau pathology and whether these components correspond with specific functional connectivity networks. Twenty-two 18F-AV-1451 PET scans of patients with amnestic Alzheimer’s disease (mean age = 66.00 ± 7.22 years, 14 males/eight females) were spatially normalized, intensity standardized to the cerebellum, and z-transformed using the mean and deviation image of a healthy control sample to assess Alzheimer’s disease-related tau pathology. First, to detect distinct tau pathology networks, the deviation maps were subjected to an independent component analysis. Second, to investigate if regions of high tau burden are associated with functional connectivity networks, we extracted the region with the maximum z-value in each of the generated tau pathology networks and used them as seeds in a subsequent resting-state functional MRI analysis, conducted in a group of healthy adults (n = 26) who were part of the 1000 Functional Connectomes Project. Third, to examine if tau pathology co-localizes with functional connectivity networks, we quantified the spatial overlap between the seed-based networks and the corresponding tau pathology network by calculating the Dice similarity coefficient. Additionally, we assessed if the tau-dependent seed-based networks correspond with known functional resting-state networks. Finally, we examined the relevance of the identified components in regard to the neuropathological Braak stages. We identified 10 independently coherent tau pathology networks with the majority showing a symmetrical bi-hemispheric expansion and coinciding with highly functionally connected brain regions such as the precuneus and cingulate cortex. A fair-to-moderate overlap was observed between the tau pathology networks and corresponding seed-based networks (Dice range: 0.13–0.57), which in turn resembled known resting-state networks, particularly the default mode network (Dice range: 0.42–0.56). Moreover, greater tau burden in the tau pathology networks was associated with more advanced Braak stages. Using the data-driven approach of an independent component analysis, we observed a set of independently coherent tau pathology networks in Alzheimer’s disease, which were associated with disease progression and coincided with functional networks previously reported to be impaired in Alzheimer’s disease. Together, our results provide novel information regarding the impact of tau pathology networks on the mechanistic pathway of Alzheimer’s disease.</style></abstract><urls><related-urls><url><style face="normal" font="default" size="100%">https://doi.org/10.1093/brain/awx353</style></url></related-urls></urls><electronic-resource-num><style face="normal" font="default" size="100%">10.1093/brain/awx353</style></electronic-resource-num><access-date><style face="normal" font="default" size="100%">2/17/2022</style></access-date></record><record><database name="neumaier.enl" path="C:\Users\b.mayer\Desktop\UKZ Bilder\neumaier.enl">neumaier.enl</database><source-app name="EndNote" version="21.4">EndNote</source-app><rec-number>4</rec-number><foreign-keys><key app="EN" db-id="avvwwzara0ssdaef0vjv92r1wtp5sxstv2vz">4</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Hoffmann, Chris</style></author><author><style face="normal" font="default" size="100%">Evcüman, Sibel</style></author><author><style face="normal" font="default" size="100%">Neumaier, Felix</style></author><author><style face="normal" font="default" size="100%">Zlatopolskiy, Boris D.</style></author><author><style face="normal" font="default" size="100%">Humpert, Swen</style></author><author><style face="normal" font="default" size="100%">Bier, Dirk</style></author><author><style face="normal" font="default" size="100%">Holschbach, Marcus</style></author><author><style face="normal" font="default" size="100%">Schulze, Annette</style></author><author><style face="normal" font="default" size="100%">Endepols, Heike</style></author><author><style face="normal" font="default" size="100%">Neumaier, Bernd</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">[18F]ALX5406: A Brain-Penetrating Prodrug for GlyT1-Specific PET Imaging</style></title><secondary-title><style face="normal" font="default" size="100%">ACS Chemical Neuroscience</style></secondary-title></titles><periodical><full-title><style face="normal" font="default" size="100%">ACS Chemical Neuroscience</style></full-title></periodical><pages><style face="normal" font="default" size="100%">3335-3346</style></pages><volume><style face="normal" font="default" size="100%">12</style></volume><number><style face="normal" font="default" size="100%">18</style></number><dates><year><style face="normal" font="default" size="100%">2021</style></year><pub-dates><date><style face="normal" font="default" size="100%">2021/09/15</style></date></pub-dates></dates><publisher><style face="normal" font="default" size="100%">American Chemical Society</style></publisher><urls><related-urls><url><style face="normal" font="default" size="100%">https://doi.org/10.1021/acschemneuro.1c00284</style></url></related-urls></urls><electronic-resource-num><style face="normal" font="default" size="100%">10.1021/acschemneuro.1c00284</style></electronic-resource-num></record><record><database name="neumaier.enl" path="C:\Users\b.mayer\Desktop\UKZ Bilder\neumaier.enl">neumaier.enl</database><source-app name="EndNote" version="21.4">EndNote</source-app><rec-number>5</rec-number><foreign-keys><key app="EN" db-id="avvwwzara0ssdaef0vjv92r1wtp5sxstv2vz">5</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Humpert, Swen</style></author><author><style face="normal" font="default" size="100%">Omrane, Mohamed A.</style></author><author><style face="normal" font="default" size="100%">Urusova, Elizaveta A.</style></author><author><style face="normal" font="default" size="100%">Gremer, Lothar</style></author><author><style face="normal" font="default" size="100%">Willbold, Dieter</style></author><author><style face="normal" font="default" size="100%">Endepols, Heike</style></author><author><style face="normal" font="default" size="100%">Krasikova, Raisa N.</style></author><author><style face="normal" font="default" size="100%">Neumaier, Bernd</style></author><author><style face="normal" font="default" size="100%">Zlatopolskiy, Boris D.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Rapid 18F-labeling via Pd-catalyzed S-arylation in aqueous medium</style></title><secondary-title><style face="normal" font="default" size="100%">Chemical Communications</style></secondary-title></titles><periodical><full-title><style face="normal" font="default" size="100%">Chemical Communications</style></full-title></periodical><pages><style face="normal" font="default" size="100%">3547-3550</style></pages><volume><style face="normal" font="default" size="100%">57</style></volume><number><style face="normal" font="default" size="100%">29</style></number><dates><year><style face="normal" font="default" size="100%">2021</style></year></dates><publisher><style face="normal" font="default" size="100%">The Royal Society of Chemistry</style></publisher><isbn><style face="normal" font="default" size="100%">1359-7345</style></isbn><abstract><style face="normal" font="default" size="100%">We report radiolabeling of thiol-containing substrates via Pd-catalyzed S-arylation with 2-[18F]fluoro-5-iodopyridine, which is readily accessible using the “minimalist” radiofluorination method. The practicality of the procedure was confirmed by preparation of a novel PSMA-specific PET-tracer as well as labeling of glutathione, Aβ oligomer-binding RD2 peptide, bovine serum albumin and PSMA I&amp;S.</style></abstract><work-type><style face="normal" font="default" size="100%">10.1039/D1CC00745A</style></work-type><urls><related-urls><url><style face="normal" font="default" size="100%">http://dx.doi.org/10.1039/D1CC00745A</style></url></related-urls></urls><electronic-resource-num><style face="normal" font="default" size="100%">10.1039/D1CC00745A</style></electronic-resource-num></record><record><database name="neumaier.enl" path="C:\Users\b.mayer\Desktop\UKZ Bilder\neumaier.enl">neumaier.enl</database><source-app name="EndNote" version="21.4">EndNote</source-app><rec-number>6</rec-number><foreign-keys><key app="EN" db-id="avvwwzara0ssdaef0vjv92r1wtp5sxstv2vz">6</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Richter, Nils</style></author><author><style face="normal" font="default" size="100%">Beckers, Nora</style></author><author><style face="normal" font="default" size="100%">Onur, Oezguer A.</style></author><author><style face="normal" font="default" size="100%">Dietlein, Markus</style></author><author><style face="normal" font="default" size="100%">Tittgemeyer, Marc</style></author><author><style face="normal" font="default" size="100%">Kracht, Lutz</style></author><author><style face="normal" font="default" size="100%">Neumaier, Bernd</style></author><author><style face="normal" font="default" size="100%">Fink, Gereon R.</style></author><author><style face="normal" font="default" size="100%">Kukolja, Juraj</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Effect of cholinergic treatment depends on cholinergic integrity in early Alzheimer’s disease</style></title><secondary-title><style face="normal" font="default" size="100%">Brain</style></secondary-title></titles><periodical><full-title><style face="normal" font="default" size="100%">Brain</style></full-title></periodical><pages><style face="normal" font="default" size="100%">903-915</style></pages><volume><style face="normal" font="default" size="100%">141</style></volume><number><style face="normal" font="default" size="100%">3</style></number><dates><year><style face="normal" font="default" size="100%">2018</style></year></dates><isbn><style face="normal" font="default" size="100%">0006-8950</style></isbn><abstract><style face="normal" font="default" size="100%">In early Alzheimer’s disease, which initially presents with progressive loss of short-term memory, neurodegeneration especially affects cholinergic neurons of the basal forebrain. Pharmacotherapy of Alzheimer’s disease therefore often targets the cholinergic system. In contrast, cholinergic pharmacotherapy of mild cognitive impairment is debated since its efficacy to date remains controversial. We here investigated the relationship between cholinergic treatment effects and the integrity of the cholinergic system in mild cognitive impairment due to Alzheimer’s disease. Fourteen patients with high likelihood of mild cognitive impairment due to Alzheimer’s disease and 16 age-matched cognitively normal adults performed an episodic memory task during functional magnetic resonance imaging under three conditions: (i) without pharmacotherapy; (ii) with placebo; and (iii) with a single dose of rivastigmine (3 mg). Cortical acetylcholinesterase activity was measured using PET with the tracer 11C-N-methyl-4-piperidyl acetate (MP4A). Cortical acetylcholinesterase activity was significantly decreased in patients relative to controls, especially in the lateral temporal lobes. Without pharmacotherapy, mild cognitive impairment was associated with less memory-related neural activation in the fusiform gyrus and impaired deactivation in the posterior cingulate cortex, relative to controls. These differences were attenuated under cholinergic stimulation with rivastigmine: patients showed increased neural activation in the right fusiform gyrus but enhanced deactivation of the posterior cingulate cortex under rivastigmine, compared to placebo. Conversely, controls showed reduced activation of the fusiform gyrus and reduced deactivation of the posterior cingulate under rivastigmine, compared to placebo. In both groups, the change in neural activation in response to rivastigmine was negatively associated with local acetylcholinesterase activity. At the behavioural level, an analysis of covariance revealed a significant group × treatment interaction in episodic memory performance when accounting for hippocampal grey matter atrophy and function. Our results indicate that rivastigmine differentially affects memory-related neural activity in patients with mild cognitive impairment and cognitively normal, age-matched adults, depending on acetylcholinesterase activity as a marker for the integrity of the cortical cholinergic system. Furthermore, hippocampal integrity showed an independent association with the response of memory performance to acetylcholinesterase inhibition.</style></abstract><urls><related-urls><url><style face="normal" font="default" size="100%">https://doi.org/10.1093/brain/awx356</style></url></related-urls></urls><electronic-resource-num><style face="normal" font="default" size="100%">10.1093/brain/awx356</style></electronic-resource-num><access-date><style face="normal" font="default" size="100%">2/17/2022</style></access-date></record><record><database name="neumaier.enl" path="C:\Users\b.mayer\Desktop\UKZ Bilder\neumaier.enl">neumaier.enl</database><source-app name="EndNote" version="21.4">EndNote</source-app><rec-number>12</rec-number><foreign-keys><key app="EN" db-id="avvwwzara0ssdaef0vjv92r1wtp5sxstv2vz">12</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Walter, N.</style></author><author><style face="normal" font="default" size="100%">Bertram, J.</style></author><author><style face="normal" font="default" size="100%">Drewes, B.</style></author><author><style face="normal" font="default" size="100%">Bahutski, V.</style></author><author><style face="normal" font="default" size="100%">Timmer, M.</style></author><author><style face="normal" font="default" size="100%">Schutz, M. B.</style></author><author><style face="normal" font="default" size="100%">Kramer, F.</style></author><author><style face="normal" font="default" size="100%">Neumaier, F.</style></author><author><style face="normal" font="default" size="100%">Endepols, H.</style></author><author><style face="normal" font="default" size="100%">Neumaier, B.</style></author><author><style face="normal" font="default" size="100%">Zlatopolskiy, B. D.</style></author></authors></contributors><auth-address><style face="normal" font="default" size="100%">Forschungszentrum Julich GmbH, Institute of Neuroscience and Medicine, Nuclear Chemistry (INM-5), Wilhelm-Johnen-Strasse, 52425, Julich, Germany. Electronic address: n.walter@fz-juelich.de.&#xD;Forschungszentrum Julich GmbH, Institute of Neuroscience and Medicine, Nuclear Chemistry (INM-5), Wilhelm-Johnen-Strasse, 52425, Julich, Germany. Electronic address: jbertra1@smail.uni-koeln.de.&#xD;Forschungszentrum Julich GmbH, Institute of Neuroscience and Medicine, Nuclear Chemistry (INM-5), Wilhelm-Johnen-Strasse, 52425, Julich, Germany. Electronic address: b.drewes@fz-juelich.de.&#xD;Forschungszentrum Julich GmbH, Institute of Neuroscience and Medicine, Nuclear Chemistry (INM-5), Wilhelm-Johnen-Strasse, 52425, Julich, Germany. Electronic address: vbaguts@yahoo.com.&#xD;University of Cologne, Faculty of Medicine and Cologne University Hospital, Center for Neurosurgery, Kerpener Strasse 62, 50937, Cologne, Germany. Electronic address: marco.timmer@uk-koeln.de.&#xD;University of Cologne, Faculty of Medicine and Cologne University Hospital, Institute of Diagnostic and Interventional Radiology, Kerpener Strasse 62, 50937, Cologne, Germany. Electronic address: markus.schuetz@uk-koeln.de.&#xD;University of Cologne, Faculty of Medicine and Cologne University Hospital, Institute of Radiochemistry and Experimental Molecular Imaging, Kerpener Strasse 62, 50937, Cologne, Germany. Electronic address: maximiliane-felicia.kraemer@uk-koeln.de.&#xD;Forschungszentrum Julich GmbH, Institute of Neuroscience and Medicine, Nuclear Chemistry (INM-5), Wilhelm-Johnen-Strasse, 52425, Julich, Germany; University of Cologne, Faculty of Medicine and Cologne University Hospital, Institute of Radiochemistry and Experimental Molecular Imaging, Kerpener Strasse 62, 50937, Cologne, Germany. Electronic address: f.neumaier@fz-juelich.de.&#xD;Forschungszentrum Julich GmbH, Institute of Neuroscience and Medicine, Nuclear Chemistry (INM-5), Wilhelm-Johnen-Strasse, 52425, Julich, Germany; University of Cologne, Faculty of Medicine and Cologne University Hospital, Institute of Radiochemistry and Experimental Molecular Imaging, Kerpener Strasse 62, 50937, Cologne, Germany; University of Cologne, Faculty of Medicine and Cologne University Hospital, Department of Nuclear Medicine, Kerpener Strasse 62, 50937, Cologne, Germany. Electronic address: heike.endepols@uk-koeln.de.&#xD;Forschungszentrum Julich GmbH, Institute of Neuroscience and Medicine, Nuclear Chemistry (INM-5), Wilhelm-Johnen-Strasse, 52425, Julich, Germany; University of Cologne, Faculty of Medicine and Cologne University Hospital, Institute of Radiochemistry and Experimental Molecular Imaging, Kerpener Strasse 62, 50937, Cologne, Germany; Max Planck Institute for Metabolism Research, Gleueler Strasse 50, 50931, Cologne, Germany. Electronic address: b.neumaier@fz-juelich.de.&#xD;Forschungszentrum Julich GmbH, Institute of Neuroscience and Medicine, Nuclear Chemistry (INM-5), Wilhelm-Johnen-Strasse, 52425, Julich, Germany; University of Cologne, Faculty of Medicine and Cologne University Hospital, Institute of Radiochemistry and Experimental Molecular Imaging, Kerpener Strasse 62, 50937, Cologne, Germany; Max Planck Institute for Metabolism Research, Gleueler Strasse 50, 50931, Cologne, Germany. Electronic address: boris.zlatopolskiy@uk-koeln.de.</style></auth-address><titles><title><style face="normal" font="default" size="100%">Convenient PET-tracer production via SuFEx (18)F-fluorination of nanomolar precursor amounts</style></title><secondary-title><style face="normal" font="default" size="100%">Eur J Med Chem</style></secondary-title></titles><periodical><full-title><style face="normal" font="default" size="100%">Eur J Med Chem</style></full-title></periodical><pages><style face="normal" font="default" size="100%">114383</style></pages><volume><style face="normal" font="default" size="100%">237</style></volume><edition><style face="normal" font="default" size="100%">20220414</style></edition><keywords><keyword><style face="normal" font="default" size="100%">*Fluorine Radioisotopes/metabolism/pharmacology</style></keyword><keyword><style face="normal" font="default" size="100%">Halogenation</style></keyword><keyword><style face="normal" font="default" size="100%">Ligands</style></keyword><keyword><style face="normal" font="default" size="100%">Nanostructures</style></keyword><keyword><style face="normal" font="default" size="100%">*Positron-Emission Tomography/methods</style></keyword><keyword><style face="normal" font="default" size="100%">*Radiopharmaceuticals/metabolism/pharmacology</style></keyword><keyword><style face="normal" font="default" size="100%">Fluorine-18</style></keyword><keyword><style face="normal" font="default" size="100%">Imaging agents</style></keyword><keyword><style face="normal" font="default" size="100%">Positron emission tomography (PET)</style></keyword><keyword><style face="normal" font="default" size="100%">Radiopharmaceuticals</style></keyword><keyword><style face="normal" font="default" size="100%">SuFEx click chemistry</style></keyword></keywords><dates><year><style face="normal" font="default" size="100%">2022</style></year><pub-dates><date><style face="normal" font="default" size="100%">Jul 5</style></date></pub-dates></dates><isbn><style face="normal" font="default" size="100%">1768-3254 (Electronic)&#xD;0223-5234 (Linking)</style></isbn><accession-num><style face="normal" font="default" size="100%">35447431</style></accession-num><abstract><style face="normal" font="default" size="100%">Recently, a protocol for radiolabeling of aryl fluorosulfates (&quot;SuFEx click radiolabeling&quot;) using ultrafast (18)F/(19)F isotopic exchange has been reported. Although promising, the original procedure turned out to be rather inefficient. However, systematic optimization of the reaction parameters allowed for development of a robust method for SuFEx radiolabeling which obviates the need for azeotropic drying, base addition and HPLC purification. The developed protocol enabled efficient (18)F-fluorination of low nanomolar amounts of aryl fluorosulfates in highly diluted solution (micromolar concentrations). It was successfully used to prepare a series of 29 (18)F-fluorosulfurylated phenols - including modified ezetimibe, alpha-tocopherol and etoposide, the two tyrosine derivatives Boc-Tyr([(18)F]FS)-OMe and H-Tyr([(18)F]FS)-OMe, the FAP-specific ligand [(18)F]FS-UAMC1110, and the DPA-714 analog [(18)F]FS-DPA - in fair to excellent yields. Preliminary evaluation demonstrated sufficient in vivo stability of radiofluorinated electron rich or neutral Boc-Tyr([(18)F]FS)-OMe), H-Tyr([(18)F]FS)-OMe and [(18)F]FS-DPA aryl fluorosulfates. Furthermore, [(18)F]FS-DPA was identified as a promising tracer for visualization of TSPO expression.</style></abstract><notes><style face="normal" font="default" size="100%">Walter, Nils&#xD;Bertram, Jan&#xD;Drewes, Birte&#xD;Bahutski, Victor&#xD;Timmer, Marco&#xD;Schutz, Markus B&#xD;Kramer, Felicia&#xD;Neumaier, Felix&#xD;Endepols, Heike&#xD;Neumaier, Bernd&#xD;Zlatopolskiy, Boris D&#xD;eng&#xD;France&#xD;2022/04/22&#xD;Eur J Med Chem. 2022 Jul 5;237:114383. doi: 10.1016/j.ejmech.2022.114383. Epub 2022 Apr 14.</style></notes><urls><related-urls><url><style face="normal" font="default" size="100%">https://www.ncbi.nlm.nih.gov/pubmed/35447431</style></url></related-urls></urls><electronic-resource-num><style face="normal" font="default" size="100%">10.1016/j.ejmech.2022.114383</style></electronic-resource-num><remote-database-name><style face="normal" font="default" size="100%">Medline</style></remote-database-name><remote-database-provider><style face="normal" font="default" size="100%">NLM</style></remote-database-provider></record><record><database name="neumaier.enl" path="C:\Users\b.mayer\Desktop\UKZ Bilder\neumaier.enl">neumaier.enl</database><source-app name="EndNote" version="21.4">EndNote</source-app><rec-number>8</rec-number><foreign-keys><key app="EN" db-id="avvwwzara0ssdaef0vjv92r1wtp5sxstv2vz">8</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Zlatopolskiy, Boris D.</style></author><author><style face="normal" font="default" size="100%">Endepols, Heike</style></author><author><style face="normal" font="default" size="100%">Krapf, Philipp</style></author><author><style face="normal" font="default" size="100%">Guliyev, Mehrab</style></author><author><style face="normal" font="default" size="100%">Urusova, Elizaveta A.</style></author><author><style face="normal" font="default" size="100%">Richarz, Raphael</style></author><author><style face="normal" font="default" size="100%">Hohberg, Melanie</style></author><author><style face="normal" font="default" size="100%">Dietlein, Markus</style></author><author><style face="normal" font="default" size="100%">Drzezga, Alexander</style></author><author><style face="normal" font="default" size="100%">Neumaier, Bernd</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Discovery of &amp;lt;sup&amp;gt;18&amp;lt;/sup&amp;gt;F-JK-PSMA-7, a PET Probe for the Detection of Small PSMA-Positive Lesions</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of Nuclear Medicine</style></secondary-title></titles><periodical><full-title><style face="normal" font="default" size="100%">Journal of Nuclear Medicine</style></full-title></periodical><pages><style face="normal" font="default" size="100%">817</style></pages><volume><style face="normal" font="default" size="100%">60</style></volume><number><style face="normal" font="default" size="100%">6</style></number><dates><year><style face="normal" font="default" size="100%">2019</style></year></dates><abstract><style face="normal" font="default" size="100%">Prostate-specific membrane antigen (PSMA), expressed by most prostate carcinomas (PCa), is a promising target for PCa imaging. The application of PSMA-specific 18F-labeled PET probes such as 18F-DCFPyL and 18F-PSMA-1007 considerably improved the accuracy of PCa tumor detection. However, there remains a need for further improvements in sensitivity and specificity. The aim of this study was the development of highly selective and specific PSMA probes with enhanced imaging properties, in comparison with 18F-DCFPyL, 18F-PSMA-1007, and 68Ga-PSMA-11. Methods: Eight novel 18F-labeled PSMA ligands were prepared. Their cellular uptake in PSMA-positive LNCaP C4–2 and PSMA-negative PC-3 cells was compared with that of 18F-DCFPyL. The most promising candidates were additionally evaluated by small-animal PET in healthy rats using PSMA-positive peripheral ganglia as a model for small PCa lesions. PET images of the ligand with the best outcome, 18F-JK-PSMA-7, were compared with those of 18F-DCFPyL, 18F-PSMA-1007, and 68Ga-PSMA-11 with respect to key image-quality parameters for the time frame 60–120 min. Results: Compared with 18F-DCFPyL, 18F-JK-PSMA-7 demonstrated increased PSMA-specific cellular uptake. Although target-to-background ratios of 18F-DCFPyL and 18F-PSMA-1007 were comparable, this parameter was higher for 18F-JK-PSMA-7 and lower for 68Ga-PSMA-11. Image acutance was significantly higher for 18F-JK-PSMA-7 and 18F-PSMA-1007 than for 18F-DCFPyL and 68Ga-PSMA-11. Image resolution was similar for all 4 tracers. 18F-PSMA-1007 demonstrated significantly higher blood protein binding and bone uptake than the other tracers. Conclusion: 18F-JK-PSMA-7 is a promising candidate for high-quality visualization of small PSMA-positive lesions. Excellent preclinical imaging properties justify further preclinical and clinical studies of this tracer.</style></abstract><urls><related-urls><url><style face="normal" font="default" size="100%">http://jnm.snmjournals.org/content/60/6/817.abstract</style></url></related-urls></urls><electronic-resource-num><style face="normal" font="default" size="100%">10.2967/jnumed.118.218495</style></electronic-resource-num></record></records></xml>