Journal
PHOTOACOUSTICS
Volume 23, Issue -, Pages -Publisher
ELSEVIER GMBH
DOI: 10.1016/j.pacs.2021.100285
Keywords
Alzheimer's disease; Amyloid-beta; Animal model; Fluorescence imaging; Multi-spectral optoacoustic tomography
Categories
Funding
- Swiss National Science Foundation [320030_179277]
- ERA-NET NEURON [32NE30_173678/1]
- Vontobel foundation
- Olga Mayenfisch Stiftung
- Synapsis foundation
- Synapsis foundation career development award [2017 CDA-03]
- Helmut Horten Stiftung and Jubiladumsstiftung von Swiss Life
- UZH Entrepreneur Fellowship of the University of Zurich [MEDEF-20-021]
- European Research Council [ERC-CoG-2015-682379]
- Swiss National Science Foundation (SNF) [320030_179277] Funding Source: Swiss National Science Foundation (SNF)
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The study introduces a novel optical detection method, CRANAD-2, which can specifically and quantitatively detect Aβ deposits in the brain of AD animal models, facilitating research on AD pathological mechanisms and monitoring potential treatments targeting Aβ deposits.
The abnormal deposition of fibrillar beta-amyloid (A beta) deposits in the brain is one of the major histopathological hallmarks of Alzheimer's disease (AD). Here, we characterized curcumin-derivative CRANAD-2 for multi-spectral optoacoustic tomography and fluorescence imaging of brain A beta deposits in the arcA beta mouse model of AD cerebral amyloidosis. CRANAD-2 showed a specific and quantitative detection of A beta fibrils in vitro, even in complex mixtures, and it is capable of distinguishing between monomeric and fibrillar forms of A beta. In vivo epifluorescence microscopy and optoacoustic tomography after intravenous CRANAD-2 administration demonstrated higher cortical retention in arcA beta compared to non-transgenic littermate mice. Immunohistochemistry showed co-localization of CRANAD-2 and A beta deposits in arcA beta mouse brain sections, thus verifying the specificity of the probe. In conclusion, we demonstrate suitability of CRANAD-2 for optical detection of A beta deposits in animal models of AD pathology, which facilitates mechanistic studies and the monitoring of putative treatments targeting A beta deposits.
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