ArticleJournal of cellular and molecular medicine2022
Elevated 4R-tau in astrocytes from asymptomatic carriers of the MAPT 10+16 intronic mutation.
Article in Journal of cellular and molecular medicine, 2022. 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, 16 citations in OpenAlex.
- Alzheimer's disease brain-derived tau extracts show differential processing and transcriptional effects in human astrocytes.iScience · 2025Article
- Mutations in PSEN1 predispose inflammation in an astrocyte model of familial Alzheimer's disease through disrupted regulated intramembrane proteolysis.Molecular neurodegeneration · 2025Article
- Astrocytic RNA editing regulates the host immune response to alpha-synuclein.Science advances · 2025Article
- Development of MAPT S305 mutation human iPSC lines exhibiting elevated 4R tau expression and functional alterations in neurons and astrocytes.Cell reports · 2024Article
- Ferritin nanocage-enabled detection of pathological tau in living human retinal cells.Scientific reports · 2024Article
- Synaptic gene expression changes in frontotemporal dementia due to themedRxiv : the preprint server for health sciences · 2024Article
- Elevated 4R-tau in astrocytes from asymptomatic carriers of the MAPT 10+16 intronic mutation.Journal of cellular and molecular medicine · 2022Article
- Astrocytes in Neurodegeneration: Inspiration From Genetics.Frontiers in neuroscience · 2022Review
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
The microtubule-associated protein tau gene (MAPT) 10+16 intronic mutation causes frontotemporal lobar degeneration (FTLD) by increasing expression of four-repeat (4R)-tau isoforms. We investigated the potential role for astrocytes in the pathogenesis of FTLD by studying the expression of 4R-tau. We derived astrocytes and neurons from induced pluripotent stem cells from two asymptomatic 10+16 carriers which, compared to controls, showed persistently increased 4R:3R-tau transcript and protein ratios in both cell types. However, beyond 300 days culture, 10+16 neurons showed less marked increase of this 4R:3R-tau transcript ratio compared to astrocytes. Interestingly, throughout maturation, both 10+16 carriers consistently displayed different 4R:3R-tau transcript and protein ratios. These elevated levels of 4R-tau in astrocytes implicate glial cells in the pathogenic process and also suggests a cell-type-specific regulation and may inform and help on treatment of pre-clinical tauopathies.
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