Tamayev et al. [52] showed that inhibition of caspase-9 activity rescues both synaptic plasticity and memory deficits in Danish dementia knock-in mice, implicating caspase-9 in the pathogenesis of the disease and suggesting that PaPE-1 by reducing caspase-9 activity could be a valid therapeutic approach to treating human dementias. The gene discussed is CASP9; the disease is dementia.