ArticleNeurobiology of aging2022
Glial profiling of human tauopathy brain demonstrates enrichment of astrocytic transcripts in tau-related frontotemporal degeneration.
Article in Neurobiology of aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- Pooled it
- Exploring the PLD1-tau interaction in Frontotemporal Dementia.bioRxiv : the preprint server for biology · 2026Article
- Proteomic networks of gray and white matter reveal tissue-specific changes in human tauopathy.Annals of clinical and translational neurology · 2024Article
- Strategies for translating proteomics discoveries into drug discovery for dementia.Neural regeneration research · 2024Review
- Determinants of astrocytic pathology in stem cell models of primary tauopathies.Acta neuropathologica communications · 2023Article
- Analysis of Potential Biomarkers in Frontal Temporal Dementia: A Bioinformatics Approach.International journal of molecular sciences · 2023Article
- Determinants of Astrocytic Pathology in Stem Cell Models of Primary Tauopathies.bioRxiv : the preprint server for biology · 2023Article
- Clusters of co-abundant proteins in the brain cortex associated with fronto-temporal lobar degeneration.Alzheimer's research & therapy · 2023Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
To understand how glia may be altered in frontotemporal degeneration with tau pathology (FTD-tau), we used a NanoString glial profiling panel to measure 770 transcripts related to glial biology in human control (n = 8), Alzheimer's disease (AD) (n = 8), and FTD-tau (n = 8) dorsolateral prefrontal cortex. Compared to control, 43 genes were upregulated and 86 genes were downregulated in the FTD-tau samples. Only 3 genes were upregulated and 2 were downregulated in AD. Pathway analysis revealed many astrocyte-, microglia-, and oligodendrocyte-related pathway scores increased in FTD-tau, while neuron-related pathway scores decreased. We compared these results to a previously published proteomic dataset containing many of the same samples and found that the targeted panel approach obtained measurements for genes whose proteins were not measured in the proteomics. Our results point to the utility of multiomic approaches and marked dysregulation of glia in FTD-tau.
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