However, together with the previous results that CLSP or CLSPCOL suppresses AD-relevant death in cultured neuronal cells in vitro [2,3,7] and neuronal death is hypothesized to occur as a final neurotoxicity manifestation after neuronal dysfunction such as synaptic loss occurs, the results in the current study suggest that the CLSPCOL therapy will also be effective against neuronal death observed in human AD cases in addition to neuronal synaptic loss. This evidence concerns the gene CALML5 and Alzheimer disease.