In animal models, lamotrigine (LTG) has shown its potential to slow the biology and clinical progression of AD: (1) reduces the glutamate release from excitatory neurons [6,23,51,58,119]; (2) decreases the expression of BACE1 [124]; (3) inhibits mTOR signaling [124]; (4) attenuates selective CA1 hippocampal neuronal loss, upregulates antiapoptotic protein Bcl-2, and stimulates neurogenesis in the granule cell layer of dentate gyrus [125]; (5) reduces amyloid plaque density [69]; and (6) improves executive dysfunction [126]. The gene discussed is BACE1; the disease is Alzheimer disease.