Further target‐based therapeutic and pathological experiments verified that modulation of the miR‐32533/CREB5 axis ameliorated or aggravated cognitive impairment, along with neurodegeneration, redox imbalance, and neuroinflammation by inhibiting or amplifying Aβ overproduction, respectively, via the BACE1‐involved amyloidogenic and ADAM10‐involved non‐amyloidogenic pathways. The gene discussed is CREB5; the disease is Cognitive impairment.