ArticleFrontiers in aging neuroscience2016
In Vivo Detection of Amyloid Plaques by Gadolinium-Stained MRI Can Be Used to Demonstrate the Efficacy of an Anti-amyloid Immunotherapy.
Article in Frontiers in aging neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Associations of amyloid-β oligomers and plaques with neuropathology in theBrain communications · 2024Article
- Age-dependent microstructure alterations in 5xFAD mice by high-resolution diffusion tensor imaging.Frontiers in neuroscience · 2022Article
- Magnetic Resonance Imaging in Animal Models of Alzheimer's Disease Amyloidosis.International journal of molecular sciences · 2021Review
- Fluorine-19 Magnetic Resonance Imaging for Detection of Amyloid β Oligomers Using a Keto Form of Curcumin Derivative in a Mouse Model of Alzheimer's Disease.Molecules (Basel, Switzerland) · 2021Article
- Amyloid-β and α-Synuclein Immunotherapy: From Experimental Studies to Clinical Trials.Frontiers in neuroscience · 2021Review
- Pyk2 overexpression in postsynaptic neurons blocks amyloid βBrain communications · 2020Article
- Assessment of pathological features in Alzheimer's disease brain tissue with a large field-of-view visible-light optical coherence microscope.Neurophotonics · 2018Article
- Contrast-enhanced MR microscopy of amyloid plaques in five mouse models of amyloidosis and in human Alzheimer's disease brains.Scientific reports · 2017Article
- Development of surface-engineered PLGA nanoparticulate-delivery system of Tet1-conjugated nattokinase enzyme for inhibition of AβInternational journal of nanomedicine · 2017Article
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Authors and funding
9 authors.
Funding
Abstract
Extracellular deposition of β amyloid plaques is an early event associated to Alzheimer's disease. Here, we have used in vivo gadolinium-stained high resolution (29(∗)29(∗)117 μm(3)) magnetic resonance imaging (MRI) to follow-up in a longitudinal way individual amyloid plaques in APP/PS1 mice and evaluate the efficacy of a new immunotherapy (SAR255952) directed against protofibrillar and fibrillary forms of Aβ. APP/PS1 mice were treated for 5 months between the age of 3.5 and 8.5 months. SAR255952 reduced amyloid load in 8.5-months-old animals, but not in 5.5-months animals compared to mice treated with a control antibody (DM4). Histological evaluation confirmed the reduction of amyloid load and revealed a lower density of amyloid plaques in 8.5-months SAR255952-treated animals. The longitudinal follow-up of individual amyloid plaques by MRI revealed that plaques that were visible at 5.5 months were still visible at 8.5 months in both SAR255952 and DM4-treated mice. This suggests that the amyloid load reduction induced by SAR255952 is related to a slowing down in the formation of new plaques rather than to the clearance of already formed plaques.
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