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Analysis of gene expression changes in amyloid-beta (ADDL) and CAT-SKL antioxidant treated primary rat neuronal cells

ChEBI2014-04-11 更新2026-07-21 收录

神经退行性机制

药物干预分子效应

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-55369 数据链接链接失效反馈

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Analysis of gene expression changes in amyloid-beta (ADDL) and CAT-SKL antioxidant treated primary rat neuronal cells

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创建时间：

2014-04-11

神经退行性机制

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

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Additional file 15 of Comparative analysis of transcriptome remodeling in plaque-associated and plaque-distant microglia during amyloid-β pathology progression in mice

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Additional file 15: Table S3. Expression values for all expressed genes (in pseudocounts), related to Fig. 2.

Figshare2022-09-26 更新20

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GM2神经节苷脂沉积症模型

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Tay-Sachs and Sandhoff diseases are lethal inborn errors of acid β-N-acetylhexosaminidase activity, characterized by lysosomal storage of GM2 ganglioside and related glycoconjugates in the nervous sys

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GRN haploinsufficiency causes frontotemporal lobar degeneration and results in microglial hyperactivation, lysosomal dysfunction and TDP-43 deposition. To understand the contribution of microglial hyp

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Analysis of gene expression changes in amyloid-beta (ADDL) and CAT-SKL antioxidant treated primary rat neuronal cells

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