We propose to repair synaptic dysfunction in Alzheimer's disease and related disorders (ADRDs) by targeting caspase-2. We have delineated the mode of action by which inhibiting caspase-2 repairs synapses, which is by blocking the breakdown of tau by caspase-2. Preventing the breakdown of tau strengthens neurotransmission at excitatory synapses, which improves learning and memory. One exciting clinical implication is that a caspase-2 inhibitor would not only improve the ability to learn and remember new information, but might also recover lost memories by fortifying synapses weakened by pathological triggers. Finally, we have found evidence of this mechanism acting in several ADRD. Therefore, it is likely that a caspase-2 inhibitor would successfully improve dementia in multiple ADRDs, which is an increasingly important consideration since most patients have more than one pathology.