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Additional file 14 of β-Amyloid induces microglial expression of GPC4 and APOE leading to increased neuronal tau pathology and toxicity

NIAID Data Ecosystem2026-05-02 收录

阿尔茨海默病机制

小胶质细胞与tau病理

数据链接：

https://figshare.com/articles/dataset/Additional_file_14_of_-Amyloid_induces_microglial_expression_of_GPC4_and_APOE_leading_to_increased_neuronal_tau_pathology_and_toxicity/30015959 数据链接链接失效反馈

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资源简介：

Supplementary Material 14

应用场景：

创建时间：

2025-08-29

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,

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ABCA7 deficiency causes neuronal dysregulation by altering mitochondrial lipid metabolism

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线粒体代谢

ABCA7 loss-of-function variants are associated with increased risk of Alzheimer's disease (AD). Using ABCA7 knockout human iPSC models generated with CRISPR/Cas9, we investigated the impacts of ABCA7

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Data Sheet 1_Western diet-induced visceral adipose tissue inflammation promotes Alzheimer’s disease pathology via microglial activation in a mouse model.docx

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饮食诱导神经炎症

IntroductionWestern diet (WD)-induced visceral adipose tissue (VAT) inflammation is characterized by adipocyte hypertrophy, hypoxia, and apoptosis. Epididymal white adipose tissue (eWAT), a representa

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The CD33 short isoform is a gain-of-function variant that enhances Aß1-42 phagocytosis in microglia I. The CD33 short isoform is a gain-of-function variant that enhances Aß1-42 phagocytosis in microglia I

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小胶质细胞吞噬功能

Background: CD33 is genetically linked to Alzheimer’s disease (AD) susceptibility through differential expression of isoforms in microglia. The role of the human CD33 short isoform (hCD33m), preferent

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Table_1_Benign Regulation of the Astrocytic Phospholipase A2-Arachidonic Acid Pathway: The Underlying Mechanism of the Beneficial Effects of Manual Acupuncture on CBF.DOC

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BackgroundThe astrocytic phospholipase A2 (PLA2)-arachidonic acid (AA) pathway is crucial in understanding the reduction of cerebral blood flow (CBF) prior to cognitive deterioration. In complementary

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Additional file 14 of β-Amyloid induces microglial expression of GPC4 and APOE leading to increased neuronal tau pathology and toxicity

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