ArticleData in brief2021
Differential gene expression data from the human central nervous system across Alzheimer's disease, Lewy body diseases, and the amyotrophic lateral sclerosis and frontotemporal dementia spectrum.
Article in Data in brief, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Astrocyte transcriptomic changes along the spatiotemporal progression of Alzheimer's disease.Nature neuroscience · 2024Article
- Exploring the globoid cell leukodystrophy protein network and therapeutic interventions.Scientific reports · 2024Article
- Distinct transcriptomic responses to Aβ plaques, neurofibrillary tangles, and APOE in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Distinct Transcriptomic Responses to Aβ plaques, Neurofibrillary Tangles, andbioRxiv : the preprint server for biology · 2023Article
- Article
- Targeting S100A4 with niclosamide attenuates inflammatory and profibrotic pathways in models of amyotrophic lateral sclerosis.Journal of neuroinflammation · 2021Article
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Authors and funding
5 authors.
Funding
Abstract
In Noori et al. [1], we hypothesized that there is a shared gene expression signature underlying neurodegenerative proteinopathies including Alzheimer's disease (AD), Lewy body diseases (LBD), and the amyotrophic lateral sclerosis and frontotemporal dementia (ALS-FTD) spectrum. To test this hypothesis, we performed a systematic review and meta-analysis of 60 human central nervous system transcriptomic datasets in the public Gene Expression Omnibus and ArrayExpress repositories, comprising a total of 2,600 AD, LBD, and ALS-FTD patients and age-matched controls which passed our stringent quality control pipeline. Here, we provide the results of differential expression analyses with data quality reports for each of these 60 datasets. This atlas of differential expression across AD, LBD, and ALS-FTD may guide future work to elucidate the pathophysiological drivers of these individual diseases as well as the common substrate of neurodegeneration.
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Registered trials
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