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Additional file 2 of Altered trafficking of Kv1-Kvβ2 leads to neuronal hyperexcitability and memory deficits in amyloid-β pathology

NIAID Data Ecosystem2026-05-10 收录

阿尔茨海默病机制

神经元离子通道

数据链接：

https://figshare.com/articles/dataset/Additional_file_2_of_Altered_trafficking_of_Kv1-Kv_2_leads_to_neuronal_hyperexcitability_and_memory_deficits_in_amyloid-_pathology/32039133 数据链接链接失效反馈

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资源简介：

Supplementary Material 2

应用场景：

创建时间：

2026-03-10

阿尔茨海默病机制

神经细胞模型

We generated ELAVL4 knockout (KO), overexpression (OE), and rescue human induced pluripotent stem cell-derived neurons to study the effect that ELAVL4 has on AD-related cellular phenotypes. To gain in

NIAID Data Ecosystem50

Table_6_Network pharmacology analysis reveals neuroprotective effects of the Qin-Zhi-Zhu-Dan Formula in Alzheimer’s disease.xlsx

网络药理学

阿尔茨海默病机制

There is yet no effective drug for Alzheimer’s disease (AD) which is one of the world’s most common neurodegenerative diseases. The Qin-Zhi-Zhu-Dan Formula (QZZD) is derived from a widely used Chinese

NIAID Data Ecosystem20

Expression data from the neuron model of Alzheimer's disease (AD) with or without treatment of recombinant human mitochondrial transcriptional factor A (rhTFAM) protein. Homo sapiens

阿尔茨海默病机制

神经退行性疾病基因表达分析

To delineate the mechanism by which hTFAM suppresses AD pathology in the neuron model of AD, we first performed microarray analyses using using RNAs prepared from PS1P117L and wild-type neurons. Next,

NIAID Data Ecosystem10

Insights into the Impact of a Membrane-Anchoring Moiety on the Biological Activities of Bivalent Compounds As Potential Neuroprotectants for Alzheimer’s Disease

神经保护剂

阿尔茨海默病机制

Bivalent compounds anchoring in different manners to the membrane were designed and biologically characterized to understand the contribution of the anchor moiety to their biological activity as neuro

Figshare2018-01-05 更新40

MEG3 activates necroptosis in human neuron xenografts modeling Alzheimer’s disease II. MEG3 activates necroptosis in human neuron xenografts modeling Alzheimer’s disease II

阿尔茨海默病机制

神经元程序性坏死

Neuronal cell loss is a defining feature of Alzheimer’s disease (AD), but the underlying mechanisms remain unclear. We xenografted human or mouse neurons into the brain of a mouse model of AD. Only hu

NIAID Data Ecosystem10

Additional file 2 of Altered trafficking of Kv1-Kvβ2 leads to neuronal hyperexcitability and memory deficits in amyloid-β pathology

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