STZ or Aβ1–42 treatment in neuronal N2A cells and cortex & hippocampal regions of rat brain exhibited the significantly augmented level of Pirh2 along with Alzheimer’s disease markers like upregulated p-Tau and β-amyloid, increased AChE activity and neuronal apoptosis. This evidence concerns the gene ACHE and early-onset autosomal dominant Alzheimer disease.