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Articles by Dan Ke
Targeting C/EBPβ/ Calbindin 1 pathway bolsters the neural resilience to tau pathology and improves tau-impaired episodic memory
Abstract Intracellular accumulation of tau protein is a defining feature of Alzheimer’s disease (AD) and is closely associated with episodic memory loss. In our previous report, we highlighted the high susceptibility of ventral hippocampal Calbindin1- neurons in the dorsal part of ventral hippocampal CA1 (dvCA1Calb1- neurons) to tau pathology in AD. However, it remains unclear whether and how dvCA1Calb1+ neurons are also vulnerable during the chronic and progressive process of AD.
Microglial CD31 suppresses Aβ clearance and promotes Alzheimer pathology in 5×FAD mice
Abstract Microglia play crucial roles in Alzheimer’s disease (AD), yet the molecular mechanisms are unclear. Here, we show that CD31, a recognized endothelial marker, is predominantly expressed in microglia but not in neurons or astrocytes, and it is significantly elevated in the brains of AD patients and mouse models.
Influence of Temperature on the Removal Efficiency of Organic Matter and Ammonia from Micro-polluted Source Water
Open AccessArticle by Lichao Nengzi 1,2,*, Haitao Li 3,*, Dan Ke 1, Xiaofeng Wu 1, Lin Meng 1, Yin Fang 3 and Qiyuan Hu 1 1 Academy of Environmental and Economics Sciences, Xichang University, Xichang 615013, China 2 School of Environment and Energy, South China University of Technology, Guangzhou 510006, China 3 College of Resources and Environment, Xichang University, Xichang 615013, China * Authors to whom correspondence should be addressed.
Human tau accumulation promotes glycogen synthase kinase-3β acetylation and thus upregulates the kinase: A vicious cycle in Alzheimer neurodegeneration
Summary Background Glycogen synthase kinase-3β (GSK-3β) is one of the most effective kinases in promoting tau hyperphosphorylation and accumulation in Alzheimer's disease (AD). However, it is not clear how GSK-3β activity is regulated during AD progression. Methods We firstly used mass spectrometry to identify the acetylation site of GSK-3β, and then established the cell and animal models of GSK-3β acetylation. Next, we conducted molecular, cell biological and behavioral tests.
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