Nature Communications (Mar 2019)
Soluble TREM2 ameliorates pathological phenotypes by modulating microglial functions in an Alzheimer’s disease model
- Li Zhong,
- Ying Xu,
- Rengong Zhuo,
- Tingting Wang,
- Kai Wang,
- Ruizhi Huang,
- Daxin Wang,
- Yue Gao,
- Yifei Zhu,
- Xuan Sheng,
- Kai Chen,
- Na Wang,
- Lin Zhu,
- Dan Can,
- Yuka Marten,
- Mitsuru Shinohara,
- Chia-Chen Liu,
- Dan Du,
- Hao Sun,
- Lei Wen,
- Huaxi Xu,
- Guojun Bu,
- Xiao-Fen Chen
Affiliations
- Li Zhong
- Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University
- Ying Xu
- Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University
- Rengong Zhuo
- Department of Traditional Chinese Medicine, School of Medicine, Xiamen University
- Tingting Wang
- Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University
- Kai Wang
- Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University
- Ruizhi Huang
- Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University
- Daxin Wang
- Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University
- Yue Gao
- Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University
- Yifei Zhu
- Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University
- Xuan Sheng
- Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University
- Kai Chen
- Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University
- Na Wang
- Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University
- Lin Zhu
- Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University
- Dan Can
- Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University
- Yuka Marten
- Department of Neuroscience, Mayo Clinic
- Mitsuru Shinohara
- Department of Neuroscience, Mayo Clinic
- Chia-Chen Liu
- Department of Neuroscience, Mayo Clinic
- Dan Du
- School of Medicine, Xiamen University
- Hao Sun
- Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University
- Lei Wen
- Department of Traditional Chinese Medicine, School of Medicine, Xiamen University
- Huaxi Xu
- Neuroscience Initiative, Sanford-Burnham-Prebys Medical Discovery Institute
- Guojun Bu
- Department of Neuroscience, Mayo Clinic
- Xiao-Fen Chen
- Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University
- DOI
- https://doi.org/10.1038/s41467-019-09118-9
- Journal volume & issue
-
Vol. 10,
no. 1
pp. 1 – 16
Abstract
TREM2 is a genetic risk factor for Alzheimer’s disease, and soluble TREM2 (sTREM2) in the CSF correlates with AD progression. Here the authors study the role of sTREM2 in a mouse model of Alzheimer’s disease, and find it reduces amyloid accumulation and increases the numbers of plaque-associated microglia which correlates with improved behavioural function in the mice.
