In EOAD, neuropeptidases that break down SP, such as neutral endopeptidase E.C.3.4.24.11 and metalloendopeptidase E.C.3.4.24.15 are disrupted [100], leading to an extended metabolic half-life of SP in the temporal cortex of patients with senile dementia, which causes the increase of SP level [101]. This evidence concerns the gene MME and dementia.