Given that Casp6 activity is highly abundant in human Alzheimer brains, that Casp6 levels in the human entorhinal cortex and hippocampal CA1 regions correlate with lower episodic and semantic memory performance in aged individuals, and that Casp6 activity leads to increased amyloid beta peptide from neurons, inhibition of Casp6, if done early enough, might be an efficient treatment against AD cognitive deficits and dementia. The gene discussed is CASP6; the disease is Cognitive impairment.