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The death of neurons derived from familial Alzheimer's disease pluripotent stem cells is no different from the death of neurons derived from normal controls

Neuronal death, a pathological hallmark of Alzheimer's Disease (AD) is seen in patients whose presenilin‐1 (PS1) mutation causes their autosomal dominant AD. We assayed markers of the apoptotic death of neurons induced from pluripotent stem cells obtained from human PS1 and non‐demented controls. Our investigation included immunofluorescent imaging, analyzing TUNEL, MAP2, Caspase 3, and GABA staining for multiple samples from different PS1 individuals at different length of culture conditions. We found no significant differences between the PS1 and control groups. These baseline observations of an in‐vitro model suggest that expression of the AD phenotype requires factors beyond standard culturing conditions. This model can be used to explore stresses on the control and PS1 cell populations that will differentiate them, providing a disease‐in‐a‐dish model for those biochemical alterations likely to express the premature apoptotic phenotype of autosomal dominant AD. Research support was provided by CIRM (California Institute of Regenerative Medicine) and HHMI (Howard Hughes Medical Institute).