TP53 and early-onset autosomal dominant Alzheimer disease: A tight regulation of p53 is critical in maintaining homeostasis and keeping a balance between its cancer-suppressive and age-promoting functions [10]. The interaction between p53 and GSK3 is hypothesized to be involved in aggregate clearance and neurodegeneration: the Alzheimer’s disease hypothesis suggests that under normal conditions, GSK3 is involved in keeping p53 levels low while under conditions of cellular stress (e.g. aggregation) p53 is stabilized, proteasomal function declines, and levels of p53 increase [40, 51].