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The link between spread of alpha-synuclein, structural connectivity alteration and neurodegeneration in a-synuclein mouse model
Elucidating the temporal and spatial relation of alpha-synuclein accumulation related pathological changes, aberrant brain structural connectivity and neurodegeneration are important for understanding the mechanism of Parkinson’s disease.
Parkinson’s disease is neuropathologically hallmarked by abnormal accumulation of alpha-synucleinopathy. Elucidating the temporal and spatial relation of alpha-synuclein accumulation related pathological changes, aberrant brain structural connectivity and neurodegeneration are important for understanding the mechanism of Parkinson’s disease. Here we aim to 1) develop novel imaging tracers for detecting brain alpha-synucleinopathy in transgenic mouse model of Parkinson’s disease. 2) elucidate the spread and development of alpha-synuclein, white matter alteration and neuronal loss cross-sectionally in alpha-synuclein mouse model of different ages. We have recently developed a non-invasive transcranial imaging pipeline for detecting amyloid-beta and tau deposits in disease models of Alzheimer’s disease using optoacoustic tomography (Ni et al 2020, Ni et al 2021, Vagenknecht et al 2021). This knowledge will be important for understanding of the disease mechanism and for developing biomarker for Parkinson’s disease with translational potential.
The experiments of project include
- In vitro screening of imaging probes using recombinant tau, amyloid-beta, alpha-synuclein fibrils
- In vitro screening of imaging probes using mouse brain slices, Immunohistochemical staining and microscopy to map the regional distribution of tauopathy, in mouse model (Leica confocal & Slide scanner).
- Data analysis of the in vivo imaging in a-synuclein mice
- ELISA, MSD assay
- Data analysis, Statistics
Reference:
1. Ni Ruiqing, Chen Zhenyue, Deán-Ben Xosé Luís, Voigt Fabian. F, Kirschenbaum Daniel, Shi Gloria, Villois Alessia, Zhou Quanyu, Crimi Alessandro, Arosio Paolo, Rudin Markus, Nitsch Roger. M, K. Nilsson Peter R., Aguzzi Adriano, Helmchen Fritjof, Klohs Jan, Razansky Daniel. (2022) Multiscale optical and optoacoustic imaging of amyloid-β deposits in mice. Nature Biomedical Engineering doi: 10.1038/s41551-022-00906-1
2. Ni Ruiqing*, Villois Alessia, Dean-Ben Xose Luis, Chen Zhenyue, Vaas Markus, Stavrakis Stavros, Shi Gloria, deMello Andrew, Ran Chongzhao, Razansky Daniel, Arosio Paolo, Klohs Jan. (2021) In-vitro and in-vivo characterization of CRANAD-2 for multi-spectral optoacoustic tomography and fluorescence imaging of amyloid-beta deposits in Alzheimer mice. Photoacoustics doi: 10.1016/j.pacs.2021.100285
3. Vagenknecht Patrick, Ono Maiko, Luzgin Artur, Ji Bin, Higuchi Makoto, Noain Daniela, Maschio Cinzia, Chen Zhenyue, Konietzko Uwe, Gerez Juan A, Riek Roland, Nitsch Roger M, Razansky Daniel, Klohs Jan, Dean-Ben Xose Luis, Ni Ruiqing* (2021) Non-invasive imaging of tau-targeted probe uptake by whole brain multi-spectral optoacoustic tomography. doi: 10.21203/rs.3.rs-845733/v1
Parkinson’s disease is neuropathologically hallmarked by abnormal accumulation of alpha-synucleinopathy. Elucidating the temporal and spatial relation of alpha-synuclein accumulation related pathological changes, aberrant brain structural connectivity and neurodegeneration are important for understanding the mechanism of Parkinson’s disease. Here we aim to 1) develop novel imaging tracers for detecting brain alpha-synucleinopathy in transgenic mouse model of Parkinson’s disease. 2) elucidate the spread and development of alpha-synuclein, white matter alteration and neuronal loss cross-sectionally in alpha-synuclein mouse model of different ages. We have recently developed a non-invasive transcranial imaging pipeline for detecting amyloid-beta and tau deposits in disease models of Alzheimer’s disease using optoacoustic tomography (Ni et al 2020, Ni et al 2021, Vagenknecht et al 2021). This knowledge will be important for understanding of the disease mechanism and for developing biomarker for Parkinson’s disease with translational potential.
The experiments of project include - In vitro screening of imaging probes using recombinant tau, amyloid-beta, alpha-synuclein fibrils - In vitro screening of imaging probes using mouse brain slices, Immunohistochemical staining and microscopy to map the regional distribution of tauopathy, in mouse model (Leica confocal & Slide scanner). - Data analysis of the in vivo imaging in a-synuclein mice - ELISA, MSD assay - Data analysis, Statistics
Reference:
1. Ni Ruiqing, Chen Zhenyue, Deán-Ben Xosé Luís, Voigt Fabian. F, Kirschenbaum Daniel, Shi Gloria, Villois Alessia, Zhou Quanyu, Crimi Alessandro, Arosio Paolo, Rudin Markus, Nitsch Roger. M, K. Nilsson Peter R., Aguzzi Adriano, Helmchen Fritjof, Klohs Jan, Razansky Daniel. (2022) Multiscale optical and optoacoustic imaging of amyloid-β deposits in mice. Nature Biomedical Engineering doi: 10.1038/s41551-022-00906-1
2. Ni Ruiqing*, Villois Alessia, Dean-Ben Xose Luis, Chen Zhenyue, Vaas Markus, Stavrakis Stavros, Shi Gloria, deMello Andrew, Ran Chongzhao, Razansky Daniel, Arosio Paolo, Klohs Jan. (2021) In-vitro and in-vivo characterization of CRANAD-2 for multi-spectral optoacoustic tomography and fluorescence imaging of amyloid-beta deposits in Alzheimer mice. Photoacoustics doi: 10.1016/j.pacs.2021.100285
3. Vagenknecht Patrick, Ono Maiko, Luzgin Artur, Ji Bin, Higuchi Makoto, Noain Daniela, Maschio Cinzia, Chen Zhenyue, Konietzko Uwe, Gerez Juan A, Riek Roland, Nitsch Roger M, Razansky Daniel, Klohs Jan, Dean-Ben Xose Luis, Ni Ruiqing* (2021) Non-invasive imaging of tau-targeted probe uptake by whole brain multi-spectral optoacoustic tomography. doi: 10.21203/rs.3.rs-845733/v1
1) To develop novel imaging tracers for detecting brain alpha-synculeinopathy in transgenic mouse model. 2) To elucidate the spread and development of alpha-synculein, white matter alteration and neuronal loss cross-sectionally in alpha-synculein mouse model of different ages.
1) To develop novel imaging tracers for detecting brain alpha-synculeinopathy in transgenic mouse model. 2) To elucidate the spread and development of alpha-synculein, white matter alteration and neuronal loss cross-sectionally in alpha-synculein mouse model of different ages.
Dr. Ruiqing Ni ni@biomed.ee.ethz.ch
Wolfgang-Paulistrasse 27 HIT E22.1,8093 Zurich
Dr. Ruiqing Ni ni@biomed.ee.ethz.ch Wolfgang-Paulistrasse 27 HIT E22.1,8093 Zurich