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Integrative approach to sporadic Alzheimer's disease: deficiency of TYROBP in a tauopathy mouse model reduces C1q and normalizes clinical phenotype while increasing spread and state of phosphorylation of tau.

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第一作者: Mickael,Audrain
第一单位: Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA.
作者单位: Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA. [1] Department of Genetics and Genomic Sciences and Icahn Institute of Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA. [2] Department of Neuroscience and McKnight Brain Institute, University of Florida, Gainesville, FL, 32610, USA. [3] Tanz Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, ON, Canada. [4] Departments of Pharmacological Sciences and Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA. [5] Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA. michelle.ehrlich@mssm.edu.;Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA. michelle.ehrlich@mssm.edu. [6] Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA. samuel.gandy@mssm.edu.;Department of Psychiatry and Alzheimer's Disease Research Center, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA. samuel.gandy@mssm.edu. [7]
DOI 10.1038/s41380-018-0258-3
PMID 30283031
发布时间 2022-12-31
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