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.
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:
医学主题词
衔接蛋白质类, 信号转导(Adaptor Proteins, Signal Transducing);阿尔茨海默病(Alzheimer Disease);淀粉样β蛋白前体(Amyloid beta-Protein Precursor);动物(Animals);动物, 基因修饰(Animals, Genetically Modified);脑(Brain);补体C1q(Complement C1q);疾病模型, 动物(Disease Models, Animal);人类(Humans);膜蛋白质类(Membrane Proteins);小鼠(Mice);小鼠, 基因敲除(Mice, Knockout);小鼠, 转基因(Mice, Transgenic);小神经胶质细胞(Microglia);表型(Phenotype);磷酰化(Phosphorylation);斑块, 淀粉样(Plaque, Amyloid);Tau病变(Tauopathies);tau蛋白质类(tau Proteins)
DOI
10.1038/s41380-018-0258-3
PMID
30283031
发布时间
2022-12-31
- 浏览4
Molecular psychiatry
1383-1397页
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