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Fang, Xiaotian T.
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Fang, X. T., Hultqvist, G., Meier, S. R., Antoni, G., Sehlin, D. & Syvänen, S. (2019). High detection sensitivity with antibody-based PET radioligand for amyloid beta in brain. NeuroImage, 184, 881-888
Öppna denna publikation i ny flik eller fönster >>High detection sensitivity with antibody-based PET radioligand for amyloid beta in brain
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2019 (Engelska)Ingår i: NeuroImage, ISSN 1053-8119, E-ISSN 1095-9572, Vol. 184, s. 881-888Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

PET imaging of amyloid-beta (A beta) deposits in brain has become an important aid in Alzheimer's disease diagnosis, and an inclusion criterion for patient enrolment into clinical trials of new anti-A beta treatments. Available PET radioligands visualizing A beta bind to insoluble fibrils, i.e. A beta plaques. Levels of prefibrillar A beta forms, e.g. soluble oligomers and protofibrils, correlate better than plaques with disease severity and these soluble species are the neurotoxic form of A beta leading to neurodegeneration. The goal was to create an antibody-based radioligand, recognizing not only fibrillary A beta , but also smaller and still soluble aggregates. We designed and expressed a small recombinant bispecific antibody construct, di-scFv 3D6-8D3, targeting the A beta N-terminus and the transferrin receptor (TfR). Natively expressed at the blood-brain barrier (BBB), TfR could thus be used as a brain-blood shuttle. Di-scFv 3D6-8D3 bound to A beta 1-40 with high affinity and to TfR with moderate affinity. Di-scFv [I-124] 3D6-8D3 was injected in two transgenic mouse models overexpressing human A beta and wild-type control mice and PET scanned at 14, 24 or 72 h after injection. Di-scFv [I-124] 3D6-8D3 was retained in brain of transgenic animals while it was cleared from wild-type lacking A beta . This difference was observed from 24 h onwards, and at 72 h, 18 months old transgenic animals, with high load of A beta pathology, displayed SUVR of 2.2-3.5 in brain while wildtype showed ratios close to unity. A subset of the mice were also scanned with [C-11] PIB. Again wt mice displayed ratios of unity while transgenes showed slightly, non-significantly, elevated SUVR of 1.2, indicating improved sensitivity with novel di-scFv [I-124] 3D6-8D3 compared with [C-11] PIB. Brain concentrations of di-scFv [I-124] 3D6-8D3 correlated with soluble A beta (p < 0.0001) but not with total A beta, i.e. plaque load (p = 0.34). We have successfully created a small bispecific antibody-based radioligand capable of crossing the BBB, subsequently binding to and visualizing intrabrain A beta in vivo. The radioligand displayed better sensitivity compared with [C-11] PIB, and brain concentrations correlated with soluble neurotoxic A beta aggregates.

Nyckelord
Alzheimer's disease, Amyloid beta, PET, Antibody-based radioligand, Transferrin receptor, Brain
Nationell ämneskategori
Radiologi och bildbehandling
Identifikatorer
urn:nbn:se:uu:diva-332464 (URN)10.1016/j.neuroimage.2018.10.011 (DOI)000449385000075 ()30300753 (PubMedID)
Forskningsfinansiär
Vetenskapsrådet, 2012-1593Vetenskapsrådet, 2017-02413
Tillgänglig från: 2017-10-27 Skapad: 2017-10-27 Senast uppdaterad: 2019-01-15Bibliografiskt granskad
Meier, S. R., Syvänen, S., Hultqvist, G., Fang, X. T., Roshanbin, S., Lannfelt, L., . . . Sehlin, D. (2018). Antibody-Based In Vivo PET Imaging Detects Amyloid-beta Reduction in Alzheimer Transgenic Mice After BACE-1 Inhibition. Journal of Nuclear Medicine, 59(12), 1885-1891
Öppna denna publikation i ny flik eller fönster >>Antibody-Based In Vivo PET Imaging Detects Amyloid-beta Reduction in Alzheimer Transgenic Mice After BACE-1 Inhibition
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2018 (Engelska)Ingår i: Journal of Nuclear Medicine, ISSN 0161-5505, E-ISSN 1535-5667, Vol. 59, nr 12, s. 1885-1891Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Visualization of amyloid-beta (A beta) pathology with PET has become an important tool for making a specific clinical diagnosis of Alzheimer disease (AD). However, the available amyloid PET radioligands, such as C-11-Pittsburgh compound B, reflect levels of insoluble A beta plaques but do not capture soluble and protofibrillar A beta forms. Furthermore, the plaque load appears to be fairly static during clinical stages of AD and may not be affected by A beta-reducing treatments. The aim of the present study was to investigate whether a novel PET radioligand based on an antibody directed toward soluble aggregates of A beta can be used to detect changes in A beta levels during disease progression and after treatment with a beta-secretase (BACE-1) inhibitor. Methods: One set of transgenic mice (tg-ArcSwe, a model of A beta pathology) aged between 7 and 16 mo underwent PET with the A beta protofibril-selective radioligand I-124-RmAb158-scFv8D3 (where RmAb is recombinant mouse monoclonal antibody and scFv is single-chain variable fragment) to follow progression of A beta pathology in the brain. A second set of tg-ArcSwe mice, aged 10 mo, were treated with the BACE-1 inhibitor NB-360 for 3 mo and compared with an untreated control group. A third set of tg-ArcSwe mice, also aged 10 mo, underwent PET as a baseline group. Brain tissue was isolated after PET to determine levels of A beta by ELISA and immunohistochemistry. Results: The concentration of I-124-RmAb158-scFv8D3, as measured in vivo with PET, increased with age and corresponded well with the ex vivo autoradiography and A beta immunohistochemistry results. Mice treated with NB-360 showed significantly lower in vivo PET signals than untreated animals and were similar to the baseline animals. The decreased I-124-RmAb158-scFv8D3 concentrations in NB-360-treated mice, as quantified with PET, corresponded well with the decreased A beta levels measured in postmortem brain. Conclusion: Several treatments for AD are in phase 2 and 3 clinical trials, but the possibility of studying treatment effects in vivo on the important, nonfibrillar, forms of A beta is limited. This study demonstrated the ability of the A beta protofibril-selective radioligand I-124-RmAb158-scFv8D3 to follow disease progression and detect treatment effects with PET imaging in tg-ArcSwe mice.

Ort, förlag, år, upplaga, sidor
SOC NUCLEAR MEDICINE INC, 2018
Nyckelord
Alzheimer's disease, positron emission tomography (PET), antibody-based radioligand, BACE-1 inhibitor NB-360, amyloid-beta
Nationell ämneskategori
Radiologi och bildbehandling
Identifikatorer
urn:nbn:se:uu:diva-372378 (URN)10.2967/jnumed.118.213140 (DOI)000452015900020 ()29853653 (PubMedID)
Tillgänglig från: 2019-01-08 Skapad: 2019-01-08 Senast uppdaterad: 2019-01-08Bibliografiskt granskad
Olsen, M., Aguilar, X., Sehlin, D., Fang, X. T., Antoni, G., Erlandsson, A. & Syvänen, S. (2018). Astroglial Responses to Amyloid-Beta Progression in a Mouse Model of Alzheimer's Disease. Molecular Imaging and Biology, 20(4), 605-614
Öppna denna publikation i ny flik eller fönster >>Astroglial Responses to Amyloid-Beta Progression in a Mouse Model of Alzheimer's Disease
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2018 (Engelska)Ingår i: Molecular Imaging and Biology, ISSN 1536-1632, E-ISSN 1860-2002, Vol. 20, nr 4, s. 605-614Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by amyloid-beta (A beta) deposition, hyperphosphorylation of tau, and neuroinflammation. Astrocytes, the most abundant glial cell type in the nervous system, respond to neurodegenerative disorders through astrogliosis, i.e., converting to a reactive inflammatory state. The aim of this study was to investigate how in vivo quantification of astrogliosis using positron emission tomography (PET) radioligand deuterium-l-[C-11]deprenyl ([C-11]DED), binding to enzyme monoamine oxidase-B (MAO-B) which is overexpressed in reactive astrocytes during AD, corresponds to expression of glial fibrillary acidic protein (GFAP) and vimentin, i.e., two well-established markers of astrogliosis, during A beta pathology progression. APP(ArcSwe) mice (n = 37) and wild-type (WT) control mice (n = 23), 2-16-month old, were used to investigate biomarkers of astrogliosis. The radioligand, [C-11]DED, was used as an in vivo marker while GFAP, vimentin, and MAO-B were used to investigate astrogliosis and macrophage-associated lectin (Mac-2) to investigate microglia/macrophage activation by immunohistochemistry of the mouse brain. A beta and GFAP levels were also measured with ELISA in brain homogenates. The intrabrain levels of aggregated A beta and reactive astrocytes were found to be elevated in APP(ArcSwe) compared with WT mice. GFAP and vimentin expression increased with age, i.e., with A beta pathology, in the APP(ArcSwe) mice. This was not the case for in vivo marker [C-11]DED that showed elevated binding of the same magnitude in APP(ArcSwe) mice compared with WT mice at both 8 and 16 months. Further, immunohistochemistry indicated that there was limited co-expression of MAO-B and GFAP. MAO-B levels are increased early in A beta pathology progression, while GFAP and vimentin appear to increase later, most likely as a consequence of abundant A beta plaque formation. Thus, [C-11]DED is a useful PET radioligand for the detection of changes in MAO-B at an early stage of AD progression but does not measure the total extent of astrogliosis at advanced stages of A beta pathology.

Ort, förlag, år, upplaga, sidor
SPRINGER, 2018
Nyckelord
PET, Amyloid-beta, Astrocytes, Astrogliosis, MAO-B, GFAP, Vimentin, [C-11]DED
Nationell ämneskategori
Neurovetenskaper Neurologi
Identifikatorer
urn:nbn:se:uu:diva-361033 (URN)10.1007/s11307-017-1153-z (DOI)000438457800010 ()29297157 (PubMedID)
Forskningsfinansiär
HjärnfondenGun och Bertil Stohnes Stiftelse
Tillgänglig från: 2018-09-21 Skapad: 2018-09-21 Senast uppdaterad: 2018-09-21Bibliografiskt granskad
Eriksson, J., Fang, X. T., Hultqvist, G., Olberg, D. E., Antoni, G., Lannfelt, L., . . . Syvänen, S. (2018). [F-18]Tetrazine-trans-cyclooctene mediated labelling of antibodies for PET imaging of amyloid-beta. Paper presented at 31st Annual Congress of the European-Association-of-Nuclear-Medicine (EANM), OCT 13-17, 2018, Dusseldorf, GERMANY. European Journal of Nuclear Medicine and Molecular Imaging, 45, S643-S643
Öppna denna publikation i ny flik eller fönster >>[F-18]Tetrazine-trans-cyclooctene mediated labelling of antibodies for PET imaging of amyloid-beta
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2018 (Engelska)Ingår i: European Journal of Nuclear Medicine and Molecular Imaging, ISSN 1619-7070, E-ISSN 1619-7089, Vol. 45, s. S643-S643Artikel i tidskrift, Meeting abstract (Övrigt vetenskapligt) Published
Ort, förlag, år, upplaga, sidor
Springer, 2018
Nationell ämneskategori
Radiologi och bildbehandling
Identifikatorer
urn:nbn:se:uu:diva-372958 (URN)000449266206054 ()
Konferens
31st Annual Congress of the European-Association-of-Nuclear-Medicine (EANM), OCT 13-17, 2018, Dusseldorf, GERMANY
Tillgänglig från: 2019-01-24 Skapad: 2019-01-24 Senast uppdaterad: 2019-01-24Bibliografiskt granskad
Sousa, J., Appel, L., Fang, X. T., Engström, M., Khalighi, M., Ahlström, H. & Lubberink, M. (2018). Quantitative accuracy of 15O-water cerebral blood flow images based on penalized likelihood reconstruction. Paper presented at 31st Annual Congress of the European-Association-of-Nuclear-Medicine (EANM), OCT 13-17, 2018, Dusseldorf, GERMANY. European Journal of Nuclear Medicine and Molecular Imaging, 45(Supplement 1), S94-S95
Öppna denna publikation i ny flik eller fönster >>Quantitative accuracy of 15O-water cerebral blood flow images based on penalized likelihood reconstruction
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2018 (Engelska)Ingår i: European Journal of Nuclear Medicine and Molecular Imaging, ISSN 1619-7070, E-ISSN 1619-7089, Vol. 45, nr Supplement 1, s. S94-S95Artikel i tidskrift, Meeting abstract (Övrigt vetenskapligt) Published
Nationell ämneskategori
Radiologi och bildbehandling
Identifikatorer
urn:nbn:se:uu:diva-373336 (URN)10.1007/s00259-018-4148-3 (DOI)000449266200165 ()
Konferens
31st Annual Congress of the European-Association-of-Nuclear-Medicine (EANM), OCT 13-17, 2018, Dusseldorf, GERMANY
Anmärkning

Meeting Abstract: OP-288

Tillgänglig från: 2019-01-14 Skapad: 2019-01-14 Senast uppdaterad: 2019-01-14Bibliografiskt granskad
Syvänen, S., Fang, X. T., Hultqvist, G., Meier, S. R., Lannfelt, L. & Sehlin, D. (2017). A bispecific Tribody PET radioligand for visualization of amyloid-beta protofibrils - a new concept for neuroimaging. NeuroImage, 148, 55-63
Öppna denna publikation i ny flik eller fönster >>A bispecific Tribody PET radioligand for visualization of amyloid-beta protofibrils - a new concept for neuroimaging
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2017 (Engelska)Ingår i: NeuroImage, ISSN 1053-8119, E-ISSN 1095-9572, Vol. 148, s. 55-63Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Antibodies are highly specific for their target molecules, but their poor brain penetrance has restricted their use as PET ligands for imaging of targets within the CNS. The aim of this study was to develop an antibody-based radioligand, using the Tribody(TM) format, for PET imaging of soluble amyloid-beta (All) protofibrils, which are suggested to cause neurodegeneration in Alzheimer's disease. Antibodies, even when expressed in smaller engineered formats, are large molecules that do not enter the brain in sufficient amounts for imaging purposes. Hence, their transport across the blood-brain barrier (BBB) needs to be facilitated, for example through interaction with the transferrin receptor (TfR). Thus, a Fab fragment of the TfR antibody 8D3 was fused with two single chain variable fragments (scFv) of the A beta protofibril selective antibody mAb158. Five Tribody proteins (A1-A5) were generated with different linkers between the Fab-8D3 and scFv-158. All proteins bound to TfR and All protofibrils in vitro. Three of the proteins (A1-A3) were radiolabeled with iodine-125 and studied ex vivo in wild-type (wt) and transgenic mice overexpressing human All. The systemic pharmacokinetics were similar with half-lives in blood of around 9 h for all three ligands. Brain concentrations at 2 h were around 1% of the injected dose per gram brain tissue, which is similar to what is observed for small molecular radioligands and at least 10-fold higher than antibodies in general. At 72 h, transgenic mice showed higher concentrations of radioactivity in the brain than wt mice (12, 15- and 16-fold for Al, A2 and A3 respectively), except in the cerebellum, an area largely devoid of A beta pathology. A3 was then labelled with iodine-124 for in vivo positron emission tomography (PET) imaging. Brain concentrations were quantified in six different regions showing a clear distinction both quantitatively and visually between wt and transgenic mice and a good correlation with A beta pathology. We have thus produced a recombinant, bispecific protein, actively transported into the brain, for PET imaging within the CNS. In a longer perspective, this technique may enable imaging of other proteins involved in neurodegenerative diseases for which imaging agents are completely lacking today.

Ort, förlag, år, upplaga, sidor
ACADEMIC PRESS INC ELSEVIER SCIENCE, 2017
Nyckelord
PET, Amyloid-beta, Antibody, Transferrin receptor, Tribody
Nationell ämneskategori
Radiologi och bildbehandling
Identifikatorer
urn:nbn:se:uu:diva-320289 (URN)10.1016/j.neuroimage.2017.01.004 (DOI)000396803100006 ()28069541 (PubMedID)
Forskningsfinansiär
Vetenskapsrådet, 2012-1593HjärnfondenTorsten Söderbergs stiftelse
Tillgänglig från: 2017-04-25 Skapad: 2017-04-25 Senast uppdaterad: 2017-04-25Bibliografiskt granskad
Fang, X., Hultqvist, G., Meier, S., Sehlin, D. & Syvänen, S. (2017). A small bispecific antibody-based construct based on bapineuzumab as a PET tracer for amyloid beta pathology in brain. Paper presented at 28th International Symposium on Cerebral Blood Flow, Metabolism and Function / 13th International Conference on Quantification of Brain Function with PET, APR 01-04, 2017, Int Soc Cerebral Blood Flow & Metab, Berlin, GERMANY. Meeting abstract
Öppna denna publikation i ny flik eller fönster >>A small bispecific antibody-based construct based on bapineuzumab as a PET tracer for amyloid beta pathology in brain
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2017 (Engelska)Ingår i: Meeting abstractArtikel i tidskrift, Meeting abstract (Övrigt vetenskapligt) Published
Nationell ämneskategori
Endokrinologi och diabetes Hematologi Neurologi
Identifikatorer
urn:nbn:se:uu:diva-331029 (URN)000400157400102 ()
Konferens
28th International Symposium on Cerebral Blood Flow, Metabolism and Function / 13th International Conference on Quantification of Brain Function with PET, APR 01-04, 2017, Int Soc Cerebral Blood Flow & Metab, Berlin, GERMANY
Anmärkning

Supplement: 1, Meeting Abstract: BPS01-1

Tillgänglig från: 2017-10-11 Skapad: 2017-10-11 Senast uppdaterad: 2017-11-08
Syvänen, S., Fang, X. T., Hultqvist, G., Falting, J., Antoni, G., Lannfelt, L. & Sehlin, D. (2017). Antibody-based PET radioligands for imaging of amyloid-beta protofibrils. Paper presented at 28th International Symposium on Cerebral Blood Flow, Metabolism and Function / 13th International Conference on Quantification of Brain Function with PET, APR 01-04, 2017, Int Soc Cerebral Blood Flow & Metab, Berlin, GERMANY. Journal of Cerebral Blood Flow and Metabolism, 37, 84-84
Öppna denna publikation i ny flik eller fönster >>Antibody-based PET radioligands for imaging of amyloid-beta protofibrils
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2017 (Engelska)Ingår i: Journal of Cerebral Blood Flow and Metabolism, ISSN 0271-678X, E-ISSN 1559-7016, Vol. 37, s. 84-84Artikel i tidskrift, Meeting abstract (Övrigt vetenskapligt) Published
Ort, förlag, år, upplaga, sidor
Sage Publications, 2017
Nationell ämneskategori
Endokrinologi och diabetes Hematologi Neurologi
Identifikatorer
urn:nbn:se:uu:diva-331033 (URN)000400157400120 ()
Konferens
28th International Symposium on Cerebral Blood Flow, Metabolism and Function / 13th International Conference on Quantification of Brain Function with PET, APR 01-04, 2017, Int Soc Cerebral Blood Flow & Metab, Berlin, GERMANY
Anmärkning

Supplement: 1, Meeting Abstract: BPS04-1.

Tillgänglig från: 2017-10-11 Skapad: 2017-10-11 Senast uppdaterad: 2017-10-11
Hultqvist, G., Syvänen, S., Fang, X. T., Lannfelt, L. & Sehlin, D. (2017). Bivalent Brain Shuttle Increases Antibody Uptake by Monovalent Binding to the Transferrin Receptor. Theranostics, 7(2), 308-318
Öppna denna publikation i ny flik eller fönster >>Bivalent Brain Shuttle Increases Antibody Uptake by Monovalent Binding to the Transferrin Receptor
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2017 (Engelska)Ingår i: Theranostics, ISSN 1838-7640, E-ISSN 1838-7640, Vol. 7, nr 2, s. 308-318Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

The blood-brain barrier (BBB) is an obstacle for antibody passage into the brain, impeding the development of immunotherapy and antibody-based diagnostics for brain disorders. In the present study, we have developed a brain shuttle for active transport of antibodies across the BBB by receptor-mediated transcytosis. We have thus recombinantly fused two single-chain variable fragments (scFv) of the transferrin receptor (TfR) antibody 8D3 to the light chains of mAb158, an antibody selectively binding to A beta protofibrils, which are involved in the pathogenesis of Alzheimer's disease (AD). Despite the two TfR binders, a monovalent interaction with TfR was achieved due to the short linkers that sterically hinder bivalent binding to the TfR dimer. The design enabled efficient receptor-mediated brain uptake of the fusion protein. Two hours after administration, brain concentrations were 2-3% of the injected dose per gram brain, comparable to small molecular drugs and 80-fold higher than unmodified mAb158. After three days, fusion protein concentrations in AD transgenic mouse brains were 9-fold higher than in wild type mice, demonstrating high in vivo specificity. Thus, our innovative recombinant design markedly increases mAb158 brain uptake, which makes it a strong candidate for improved Aa immunotherapy and as a PET radioligand for early diagnosis and evaluation of treatment effect in AD. Moreover, this approach could be applied to any target within the brain.

Ort, förlag, år, upplaga, sidor
IVYSPRING INT PUBL, 2017
Nyckelord
BBB shuttle, TfR, antibodies, Alzheimer's disease, immunotherapy, PET
Nationell ämneskategori
Geriatrik
Identifikatorer
urn:nbn:se:uu:diva-319779 (URN)10.7150/thno.17155 (DOI)000396555900006 ()28042336 (PubMedID)
Forskningsfinansiär
Vetenskapsrådet, 2012-1593 2012-2172HjärnfondenStiftelsen Gamla TjänarinnorMagnus Bergvalls Stiftelse
Tillgänglig från: 2017-04-12 Skapad: 2017-04-12 Senast uppdaterad: 2017-11-29Bibliografiskt granskad
Fang, X. T., Eriksson, J., Antoni, G., Yngve, U., Cato, L., Lannfelt, L., . . . Syvänen, S. (2017). Brain mGluR5 in mice with amyloid beta pathology studied with in vivo [(11)C]ABP688 PET imaging and ex vivo immunoblotting. Neuropharmacology, 113(Pt A), 293-300, Article ID S0028-3908(16)30459-2.
Öppna denna publikation i ny flik eller fönster >>Brain mGluR5 in mice with amyloid beta pathology studied with in vivo [(11)C]ABP688 PET imaging and ex vivo immunoblotting
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2017 (Engelska)Ingår i: Neuropharmacology, ISSN 0028-3908, E-ISSN 1873-7064, Vol. 113, nr Pt A, s. 293-300, artikel-id S0028-3908(16)30459-2Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Alzheimer's disease (AD) is characterized by aggregation of amyloid beta (Aβ) into insoluble plaques. Intermediates, Aβ oligomers (Aβo), appear to be the mechanistic cause of disease. The de facto PET AD ligand, [(11)C]PIB, binds and visualizes Aβ plaque load, which does not correlate well with disease severity. Therefore, finding a dynamic target that changes with pathology progression in AD is of great interest. Aβo alter synaptic plasticity, inhibit long-term potentiation, and facilitate long-term depression; key mechanisms involved in memory and learning. In order to convey these neurotoxic effects, Aβo requires interaction with the metabotropic glutamate 5 receptor (mGluR5). The aim was to investigate in vivo mGluR5 changes in an Aβ pathology model using PET. Wild type C57/BL6 (wt) and AβPP transgenic mice (tg-ArcSwe), 4, 8, and 16 months old, were PET scanned with [(11)C]ABP688, which is highly specific to mGluR5, to investigate changes in mGluR5. Mouse brains were extracted postscan and mGluR5 and Aβ protofibril levels were assessed with immunoblotting and ELISA respectively. Receptor-dense brain regions (hippocampus, thalamus, and striatum) displayed higher [(11)C]ABP688 concentrations corresponding to mGluR5 expression pattern. Mice had similar uptake levels of [(11)C]ABP688 regardless of genotype or age. Immunoblotting revealed general decline in mGluR5 expression and elevated levels of mGluR5 in 16 months old tg-ArcSwe compared with wt mice. [(11)C]ABP688 could visualize mGluR5 in the mouse brain. In conclusion, mGluR5 levels were found to decrease with age and tended to be higher in tg-ArcSwe compared with wt mice, however these changes could not be quantified with PET.

Nyckelord
Alzheimer's disease, PET, [(11)C]ABP688, mGluR5
Nationell ämneskategori
Geriatrik Radiologi och bildbehandling Neurologi Farmakologi och toxikologi
Identifikatorer
urn:nbn:se:uu:diva-317721 (URN)10.1016/j.neuropharm.2016.10.009 (DOI)000390502200028 ()27743932 (PubMedID)
Tillgänglig från: 2017-03-17 Skapad: 2017-03-17 Senast uppdaterad: 2018-01-13Bibliografiskt granskad
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