ArticleCellular and molecular life sciences : CMLS2025
Presenilin 1 E280A mutation induces dysfunctional astrocytic phenotype in menstrual stromal-derived astrocyte-like cells.
Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Neuroprotective Potential ofBiomolecules · 2026Article
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Authors and funding
5 authors.
Funding
Abstract
Familial Alzheimer's disease (FAD) is a progressive neurodegenerative disorder associated with loss of cholinergic neurons, intra- and extracellular accumulation of amyloid beta (iAβ, eAβ), hyperphosphorylated tau, and neuroinflammation i.e., reactive glia. The precise contribution of astrocytes to neurodegeneration in FAD is still incompletely understood. Therefore, there is a need for a reliable and simple in vitro cell culture model of neuroinflammation. The aim of the present investigation was to determine the pathophysiological behavior of astrocyte-like cells (ALCs) derived from wild-type (WT) and PSEN1 E280A menstrual stromal cells (MenSCs). We found that WT and PSEN1 E280A MenSCs displayed similar cellular mesenchymal lineage markers and similar capacity to differentiate into mesenchymal lineage osteocytes, adipocytes, and chondrocytes. In addition, WT and mutant ALCs exhibited similar percentages of astrocyte lineage markers such as GFAP+ (~ 90%) and S100β+ (70%). However, compared to WT ALCs, PSEN1 E280A ALCs (i) showed a complete lack of response to Glu-induced Ca
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