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000256590 037__ $$aDZNE-2023-00348
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000256590 1001_ $$aBallweg, Anna$$b0
000256590 245__ $$a[18F]F-DED PET imaging of reactive astrogliosis in neurodegenerative diseases: preclinical proof of concept and first-in-human data.
000256590 260__ $$aLondon$$bBioMed Central$$c2023
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000256590 520__ $$aReactive gliosis is a common pathological hallmark of CNS pathology resulting from neurodegeneration and neuroinflammation. In this study we investigate the capability of a novel monoamine oxidase B (MAO-B) PET ligand to monitor reactive astrogliosis in a transgenic mouse model of Alzheimer`s disease (AD). Furthermore, we performed a pilot study in patients with a range of neurodegenerative and neuroinflammatory conditions.A cross-sectional cohort of 24 transgenic (PS2APP) and 25 wild-type mice (age range: 4.3-21.0 months) underwent 60 min dynamic [18F]fluorodeprenyl-D2 ([18F]F-DED), static 18 kDa translocator protein (TSPO, [18F]GE-180) and β-amyloid ([18F]florbetaben) PET imaging. Quantification was performed via image derived input function (IDIF, cardiac input), simplified non-invasive reference tissue modelling (SRTM2, DVR) and late-phase standardized uptake value ratios (SUVr). Immunohistochemical (IHC) analyses of glial fibrillary acidic protein (GFAP) and MAO-B were performed to validate PET imaging by gold standard assessments. Patients belonging to the Alzheimer's disease continuum (AD, n = 2), Parkinson's disease (PD, n = 2), multiple system atrophy (MSA, n = 2), autoimmune encephalitis (n = 1), oligodendroglioma (n = 1) and one healthy control underwent 60 min dynamic [18F]F-DED PET and the data were analyzed using equivalent quantification strategies.We selected the cerebellum as a pseudo-reference region based on the immunohistochemical comparison of age-matched PS2APP and WT mice. Subsequent PET imaging revealed that PS2APP mice showed elevated hippocampal and thalamic [18F]F-DED DVR when compared to age-matched WT mice at 5 months (thalamus: + 4.3%; p = 0.048), 13 months (hippocampus: + 7.6%, p = 0.022) and 19 months (hippocampus: + 12.3%, p < 0.0001; thalamus: + 15.2%, p < 0.0001). Specific [18F]F-DED DVR increases of PS2APP mice occurred earlier when compared to signal alterations in TSPO and β-amyloid PET and [18F]F-DED DVR correlated with quantitative immunohistochemistry (hippocampus: R = 0.720, p < 0.001; thalamus: R = 0.727, p = 0.002). Preliminary experience in patients showed [18F]F-DED VT and SUVr patterns, matching the expected topology of reactive astrogliosis in neurodegenerative (MSA) and neuroinflammatory conditions, whereas the patient with oligodendroglioma and the healthy control indicated [18F]F-DED binding following the known physiological MAO-B expression in brain.[18F]F-DED PET imaging is a promising approach to assess reactive astrogliosis in AD mouse models and patients with neurological diseases.
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000256590 650_7 $$2Other$$aAstrocytes
000256590 650_7 $$2Other$$aDeprenyl
000256590 650_7 $$2Other$$aMAO-B
000256590 650_7 $$2Other$$aPET
000256590 650_7 $$2NLM Chemicals$$aAmyloid beta-Peptides
000256590 650_7 $$0EC 1.4.3.4$$2NLM Chemicals$$aMonoamine Oxidase
000256590 650_7 $$2NLM Chemicals$$aTSPO protein, human
000256590 650_7 $$2NLM Chemicals$$aReceptors, GABA
000256590 650_2 $$2MeSH$$aHumans
000256590 650_2 $$2MeSH$$aMice
000256590 650_2 $$2MeSH$$aAnimals
000256590 650_2 $$2MeSH$$aInfant
000256590 650_2 $$2MeSH$$aGliosis: pathology
000256590 650_2 $$2MeSH$$aNeurodegenerative Diseases: metabolism
000256590 650_2 $$2MeSH$$aOligodendroglioma: metabolism
000256590 650_2 $$2MeSH$$aOligodendroglioma: pathology
000256590 650_2 $$2MeSH$$aCross-Sectional Studies
000256590 650_2 $$2MeSH$$aPilot Projects
000256590 650_2 $$2MeSH$$aAlzheimer Disease: pathology
000256590 650_2 $$2MeSH$$aPositron-Emission Tomography: methods
000256590 650_2 $$2MeSH$$aAmyloid beta-Peptides: metabolism
000256590 650_2 $$2MeSH$$aBrain: metabolism
000256590 650_2 $$2MeSH$$aMice, Transgenic
000256590 650_2 $$2MeSH$$aInflammation: metabolism
000256590 650_2 $$2MeSH$$aMonoamine Oxidase: metabolism
000256590 650_2 $$2MeSH$$aReceptors, GABA: metabolism
000256590 7001_ $$0P:(DE-2719)9001221$$aKlaus, Carolin$$b1$$eFirst author$$udzne
000256590 7001_ $$aVogler, Letizia$$b2
000256590 7001_ $$0P:(DE-2719)9001160$$aKatzdobler, Sabrina$$b3$$udzne
000256590 7001_ $$0P:(DE-2719)9001653$$aWind, Karin$$b4$$udzne
000256590 7001_ $$0P:(DE-2719)9001654$$aZatcepin, Artem$$b5$$udzne
000256590 7001_ $$aZiegler, Sibylle I$$b6
000256590 7001_ $$aSecgin, Birkan$$b7
000256590 7001_ $$aEckenweber, Florian$$b8
000256590 7001_ $$aBohr, Bernd$$b9
000256590 7001_ $$0P:(DE-2719)9002620$$aBernhardt, Maximilian Alexander$$b10$$udzne
000256590 7001_ $$0P:(DE-2719)9001214$$aFietzek, Urban$$b11$$udzne
000256590 7001_ $$0P:(DE-2719)9001808$$aRauchmann, Boris-Stephan$$b12$$eLast author$$udzne
000256590 7001_ $$aStoecklein, Sophia$$b13
000256590 7001_ $$aQuach, Stefanie$$b14
000256590 7001_ $$aBeyer, Leonie$$b15
000256590 7001_ $$0P:(DE-HGF)0$$aScheifele, Maximilian$$b16
000256590 7001_ $$aSimmet, Marcel$$b17
000256590 7001_ $$aJoseph, Emanuel$$b18
000256590 7001_ $$aLindner, Simon$$b19
000256590 7001_ $$aBerg, Isabella$$b20
000256590 7001_ $$aKoglin, Norman$$b21
000256590 7001_ $$aMueller, Andre$$b22
000256590 7001_ $$aStephens, Andrew W$$b23
000256590 7001_ $$aBartenstein, Peter$$b24
000256590 7001_ $$aTonn, Joerg C$$b25
000256590 7001_ $$aAlbert, Nathalie L$$b26
000256590 7001_ $$aKümpfel, Tania$$b27
000256590 7001_ $$aKerschensteiner, Martin$$b28
000256590 7001_ $$0P:(DE-2719)2812234$$aPerneczky, Robert$$b29$$udzne
000256590 7001_ $$0P:(DE-2719)2811659$$aLevin, Johannes$$b30$$udzne
000256590 7001_ $$0P:(DE-2719)9002242$$aPaeger, Lars$$b31$$udzne
000256590 7001_ $$0P:(DE-2719)2810441$$aHerms, Jochen$$b32$$udzne
000256590 7001_ $$0P:(DE-2719)9001539$$aBrendel, Matthias$$b33$$eLast author$$udzne
000256590 773__ $$0PERI:(DE-600)2156455-3$$a10.1186/s12974-023-02749-2$$gVol. 20, no. 1$$n1$$p68$$tJournal of neuroinflammation$$v20$$x1742-2094$$y2023
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