000131879 001__ 131879 000131879 005__ 20250129092402.0 000131879 0247_ $$2DOI$$a10.3413/Nukmed-2012020001 000131879 0247_ $$2pmid$$apmid:22434155 000131879 0247_ $$2WOS$$aWOS:000303267400002 000131879 037__ $$aFZJ-2013-01139 000131879 082__ $$a610 000131879 1001_ $$0P:(DE-HGF)0$$aSabri, O$$b0$$eCorresponding author 000131879 1112_ $$a50. Jahrestagung der Deutschen Gesellschaft für Nuklearmedizin$$cBremen$$d2012-04-25 - 2012-04-28$$gDGN2012$$wGermany 000131879 245__ $$aFirst in man study with the new radioligand F-18-Flubatine to image alpha4beta2 cerebral nicotinic acetylcholine receptors (nAChRs) in early Alzheimer’s disease (AD) with PET 000131879 260__ $$aStuttgart$$bSchattauer$$c2012 000131879 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1360765077_27738 000131879 3367_ $$2DataCite$$aOutput Types/Journal article 000131879 3367_ $$00$$2EndNote$$aJournal Article 000131879 3367_ $$2BibTeX$$aARTICLE 000131879 3367_ $$2ORCID$$aJOURNAL_ARTICLE 000131879 3367_ $$2DRIVER$$aarticle 000131879 500__ $$3POF3_Assignment on 2016-02-29 000131879 520__ $$aZiel/Aim: Using F-18-A85380 (2FA) PET we recently demonstrated significant cerebral nAChR declines in early AD which correlated significantly with the loss of cognitive function (1-2). However, 2FA is not well suited in clinical routine use because of slow kinetics, acquisition times up to 7 hours, and limited nAChR selectivity. Thus, we developed the new tracer F-18-Flubatine, an epibatidine derivative without toxicity in humans formerly named as F-18-NCFHEB (3) and report here on the worldwide first human Flubatine-PET results. Methodik/Methods: 16 mild AD patients (NINCDS-ADRDA, age 74.4±6.6, MMSE 23.7±2.8) and 11 age-matched healthy controls (HCs, MMSE 28.5±0.9), all nonsmokers and nave for central acting medication, underwent Flubatine- PET (370 MBq, 3D-acquisition, ECAT Exact HR+). Dynamic 0-270min p.i. scans were acquired and corrected for motion (SPM2). Kinetic modeling was applied to 29 brain VOI-based tissue-activity curves (VOIs defined on individual MRI) using a one-tissue compartment model with measured arterial input function. Total distribution volume (DV) and binding potential (BP, reference region: corpus callosum) were used to characterize specific binding. Ergebnisse/Results: Image quality of Flubatine scans was clearly superior to 2FA, and a 20 minutes scan already adequate for visual analysis. All 29 regions were well described with one-tissue compartment. PET data acquired over only 90 minutes were sufficient to estimate all kinetic parameters precisely indicating a fast receptor binding kinetic (much faster than for 2FA). DVs in HCs increase as expected with receptor density: Corpus callosum (DV: 4.81±0.32), posterior cingulate (8.92±0.66), temporal (9.03±0.44), pons (11.00±1.19), thalamus (24.32±2.96). The AD patients showed extensive BP reductions in frontal, parietal, temporal, anterior and posterior cingulate cortices, caudate, and midbrain (all p<0.05) compared to HCs. There was significant correlation between nAChR reductions and cognitive declines in posterior cingulate, parietal, and temporal cortices, as well as in pons and cerebellum (p<0.05, all r> 0.41). Schlussfolgerungen/Conclusions: Due to the significant shorter acquisition time and superior image quality Flubatine appears to be a much more valuable tracer than 2FA to image nAChRs in humans. Early AD patients show significant declines of nAChRs in brain regions typically affected by AD pathology which correlate well with the corresponding cognitive declines. These results indicate that Flubatine-PET has a great potential as a biomarker for early AD diagnosis. Literatur/References: (1) Sabri et al. Eur J Nucl Med Mol Imaging 2008; 35 (Suppl. 1): 30-45 (2) Kendziorra et al., Eur J Nucl Med Mol Imaging 2011; 38: 515-525 (3) Brust et al. Synapse 2008; 62: 205-218 This trial is granted by the German Federal Ministry of Education and Research (BMBF-Nr. 01EZ0820) 000131879 536__ $$0G:(DE-HGF)POF2-333$$a333 - Pathophysiological Mechanisms of Neurological and Psychiatric Diseases (POF2-333)$$cPOF2-333$$fPOF II$$x0 000131879 536__ $$0G:(DE-Juel1)BMBF-01EZ0822$$aBMBF-01EZ0822 - NorChloro-Fluoro HomoEpiBatidin (NCFHEB) ein potentieller Positronen-Emission Tomographie-(PET) Marker der frühen Alzheimer-Demenz (BMBF-01EZ0822)$$cBMBF-01EZ0822$$x1 000131879 7001_ $$0P:(DE-HGF)0$$aWilke, S$$b1 000131879 7001_ $$0P:(DE-HGF)0$$aGräf, S$$b2 000131879 7001_ $$0P:(DE-HGF)0$$aLengler, U$$b3 000131879 7001_ $$0P:(DE-HGF)0$$aGertz, H$$b4 000131879 7001_ $$0P:(DE-HGF)0$$aSchönknecht, P$$b5 000131879 7001_ $$0P:(DE-HGF)0$$aHabermann, B$$b6 000131879 7001_ $$0P:(DE-HGF)0$$aBecker, G$$b7 000131879 7001_ $$0P:(DE-HGF)0$$aLuthardt, J$$b8 000131879 7001_ $$0P:(DE-HGF)0$$aPatt, M$$b9 000131879 7001_ $$0P:(DE-HGF)0$$aKendziorra, K$$b10 000131879 7001_ $$0P:(DE-HGF)0$$aMeyer, P$$b11 000131879 7001_ $$0P:(DE-HGF)0$$aHesse, S$$b12 000131879 7001_ $$0P:(DE-HGF)0$$aBarthel, H$$b13 000131879 7001_ $$0P:(DE-HGF)0$$aSteinbach, J$$b14 000131879 7001_ $$0P:(DE-Juel1)133954$$aWagenknecht, Gudrun$$b15 000131879 7001_ $$0P:(DE-HGF)0$$aHöpping, A$$b16 000131879 7001_ $$0P:(DE-HGF)0$$aHegerl, U$$b17 000131879 7001_ $$0P:(DE-HGF)0$$aBrust, P$$b18 000131879 773__ $$0PERI:(DE-600)2030804-8$$a10.3413/Nukmed-2012020001$$n2$$pA33$$tNuklearmedizin$$v51$$x0029-5566 000131879 909CO $$ooai:juser.fz-juelich.de:131879$$pVDB 000131879 9141_ $$y2012 000131879 915__ $$0StatID:(DE-HGF)0010$$2StatID$$aJCR/ISI refereed 000131879 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR 000131879 915__ $$0StatID:(DE-HGF)0110$$2StatID$$aWoS$$bScience Citation Index 000131879 915__ $$0StatID:(DE-HGF)0111$$2StatID$$aWoS$$bScience Citation Index Expanded 000131879 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection 000131879 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bThomson Reuters Master Journal List 000131879 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS 000131879 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline 000131879 915__ $$0StatID:(DE-HGF)1110$$2StatID$$aDBCoverage$$bCurrent Contents - Clinical Medicine 000131879 9101_ $$0I:(DE-Juel1)ZEA-2-20090406$$6P:(DE-Juel1)133954$$aZentralinstitut für Elektronik$$b15$$kZEA-2 000131879 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-Juel1)133954$$aForschungszentrum Jülich GmbH$$b15$$kFZJ 000131879 9132_ $$0G:(DE-HGF)POF3-579H$$1G:(DE-HGF)POF3-570$$2G:(DE-HGF)POF3-500$$aDE-HGF$$bKey Technologies$$lDecoding the Human Brain$$vAddenda$$x0 000131879 9131_ $$0G:(DE-HGF)POF2-333$$1G:(DE-HGF)POF2-330$$2G:(DE-HGF)POF2-300$$3G:(DE-HGF)POF2$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lFunktion und Dysfunktion des Nervensystems$$vPathophysiological Mechanisms of Neurological and Psychiatric Diseases$$x0 000131879 9201_ $$0I:(DE-Juel1)ZEL-20090406$$kZEL$$lZentralinstitut für Elektronik$$x0 000131879 9201_ $$0I:(DE-Juel1)ZEA-2-20090406$$kZEA-2$$lZentralinstitut für Elektronik$$x1 000131879 980__ $$ajournal 000131879 980__ $$aVDB 000131879 980__ $$aUNRESTRICTED 000131879 980__ $$aI:(DE-Juel1)ZEL-20090406 000131879 980__ $$aI:(DE-Juel1)ZEA-2-20090406 000131879 981__ $$aI:(DE-Juel1)PGI-4-20110106 000131879 981__ $$aI:(DE-Juel1)ZEA-2-20090406