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Human and mouse single-nucleus transcriptomics reveal TREM2-dependent and -independent cellular responses in Alzheimer’s disease

NIAID Data Ecosystem2026-03-11 收录

神经退行性疾病单细胞转录组

阿尔茨海默病分子机制

数据链接：

https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE140511 数据链接链接失效反馈

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资源简介：

This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

应用场景：

创建时间：

2020-03-31

阿尔茨海默病分子机制

神经药物靶点

Despite extensive research on Alzheimer’s disease (AD), its diagnosis and treatment remain challenging, and no effective therapies are currently available. Amyloid β (Aβ) extracellular plaques and int

NIAID Data Ecosystem30

X‑ray Crystallographic Structures of a Trimer, Dodecamer, and Annular Pore Formed by an Aβ 17–36 β‑Hairpin

淀粉样蛋白β结构

阿尔茨海默病分子机制

High-resolution structures of oligomers formed by the β-amyloid peptide Aβ are needed to understand the molecular basis of Alzheimer’s disease and develop therapies. This paper presents the X-ray crys

NIAID Data Ecosystem20

CNS SIRT3 Expression Is Altered by Reactive Oxygen Species and in Alzheimer’s Disease

阿尔茨海默病分子机制

线粒体应激响应

Progressive mitochondrial dysfunction contributes to neuronal degeneration in age-mediated disease. An essential regulator of mitochondrial function is the deacetylase, sirtuin 3 (SIRT3). Here we inve

Figshare2016-01-19 更新20

Transcriptional response by murine microglia in Alzheimer's disease

阿尔茨海默病分子机制

胶质细胞转录组学

Murine N9 microglial cells were treated with LPS (1Âµg/ml) for 6 hours. Comparing LPS treated vs. untreated microglial cells will expand upon our previous study comparing the microgial transcriptional

NIAID Data Ecosystem30

Additional file 1 of P2X7 receptor inhibition ameliorates ubiquitin–proteasome system dysfunction associated with Alzheimer’s disease

阿尔茨海默病分子机制

蛋白酶体调控

Additional file 1: SupplementaryFigure 1. P2X7R activationcauses a time- and dose-dependent reduction in UPS activity in N2a cells butdoes not affect the cellular translation or transcription capaciti

Figshare2023-06-08 更新20

Human and mouse single-nucleus transcriptomics reveal TREM2-dependent and -independent cellular responses in Alzheimer’s disease

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