In mature neurons derived from iPSCs by direct differentiation, a significant drop in Lamin B1 protein expression can be seen for T21 and familial early-onset Alzheimer’s disease (searching specifically for LMNB1 in SuppTables 1A-C82), which aligns with our models and interpretation, but also with some of our unpublished data suggesting an additional role of Aβ aggregate toxicity on the degree of senescence of mature neurons. This evidence concerns the gene LMNB1 and early-onset autosomal dominant Alzheimer disease.