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Specific Uptake of an Amyloid-beta Protofibril-Binding Antibody-Tracer in A beta PP Transgenic Mouse Brain
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics. (Rudbeck Laboratory)
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics. (Rudbeck Laboratory)
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics. (Rudbeck Laboratory)
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Medicinal Chemistry, Preclinical PET Platform. (Rudbeck Laboratory)
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2013 (English)In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 37, no 1, 29-40 p.Article in journal (Refereed) Published
Abstract [en]

Evidence suggests that amyloid-beta (A beta) protofibrils/oligomers are pathogenic agents in Alzheimer's disease (AD). Unfortunately, techniques enabling quantitative estimates of these species in patients or patient samples are still rather limited. Here we describe the in vitro and ex vivo characteristics of a new antibody-based radioactive ligand, [I-125]mAb158, which binds to A beta protofibrils with high affinity. [I-125]mAb158 was specifically taken up in brain of transgenic mice expressing amyloid-beta protein precursor (A beta PP) as shown ex vivo. This was in contrast to [I-125]mAb-Ly128 which does not bind to A beta. The uptake of intraperitoneally-administered [I-125]mAb158 into the brain was age- and time-dependent, and saturable in A beta PP transgenic mice with modest A beta deposition. Brain uptake was also found in young A beta PP transgenic mice that were devoid of A beta deposits, suggesting that [I-125]mAb158 targets soluble A beta protofibrils. The radioligand was diffusely located in the parenchyma, sometimes around senile plaques and only occasionally colocalized with cerebral amyloid angiopathy. A refined iodine-124-labeled version of mAb158 with much improved blood-brain barrier passage and a shorter plasma half-life might be useful for PET imaging of A beta protofibrils.

Place, publisher, year, edition, pages
2013. Vol. 37, no 1, 29-40 p.
Keyword [en]
Alzheimer's disease, amyloid-beta protofibrils, antibody, brain uptake, positron emission tomography, transgenic mice
National Category
Neurology
Identifiers
URN: urn:nbn:se:uu:diva-207656DOI: 10.3233/JAD-130029ISI: 000323487300005OAI: oai:DiVA.org:uu-207656DiVA: diva2:648997
Note

De 2 första författarna delar förstaförfattarskapet.

Available from: 2013-09-17 Created: 2013-09-17 Last updated: 2017-12-06

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Magnusson, KristinaSehlin, DagSyvänen, StinaTolmachev, VladimirAntoni, GunnarLannfelt, LarsHall, HåkanNilsson, Lars N. G.

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Magnusson, KristinaSehlin, DagSyvänen, StinaTolmachev, VladimirAntoni, GunnarLannfelt, LarsHall, HåkanNilsson, Lars N. G.
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GeriatricsPreclinical PET PlatformBiomedical Radiation Sciences
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