Increase in membrane cholesterol of neurons in culture recapitulates AlzheimerM-bM-^@M-^Ys disease early phenotypes.

ChEBI2015-01-15 更新2026-07-21 收录

阿尔茨海默病机制

神经元胆固醇代谢

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https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-46221 数据链接链接失效反馈

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Increase in membrane cholesterol of neurons in culture recapitulates AlzheimerM-bM-^@M-^Ys disease early phenotypes.

创建时间：

2015-01-15

CRISPRi Screening of Enhancers in Human Primary Astrocytes Identifies Regulatory Circuitry Disrupted in Alzheimer’s Disease [RNA-seq]

基因调控网络

阿尔茨海默病机制

We used CROP-seq to perform a high-throughput, parallel screen of 979 candidate enhancer perturbations in normal human astrocytes (NHAs), a primary cell-line. We identified the target gene(s) for 145

NIAID Data Ecosystem50

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

阿尔茨海默病机制

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

NIAID Data Ecosystem30

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

阿尔茨海默病机制

针刺调控脑血流

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

NIAID Data Ecosystem10

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 Ecosystem30

ABCA7 deficiency causes neuronal dysregulation by altering mitochondrial lipid metabolism

阿尔茨海默病机制

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

NIAID Data Ecosystem20

Increase in membrane cholesterol of neurons in culture recapitulates AlzheimerM-bM-^@M-^Ys disease early phenotypes.

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