Patient-derived astrocytes, but not those derived from isogenic corrected lines or healthy controls, presented alterations in Aβ metabolism since, although diseased astrocytes produced similar levels of total Aβ, PSEN1-mutant astrocytes increased 5-fold Aβ1–42 peptide secretion and showed reduced capacity of Aβ internalization and degradation, suggesting that PSEN1-mutant astrocytes could directly contribute to enhance Aβ load in AD brains. This evidence concerns the gene PSEN1 and Alzheimer disease.