The treatment with 11 of APPSw, animal model of AD, reversed memory and learning deficits aftera short period of treatment, sustained beneficial effects on cognitivefunctions even after 1 month of treatment cessation, indicating apotential for disease modification, restored synaptic integrity, andincreased EAAT2 expression via the translational rather than the transcriptionalactivation mechanism, resolving the central problem of reduced EAAT2expression.139 Other translational activatorsare sulbactam, amitriptyline, riluzole, GPI-1046, and MS-153. The gene discussed is SLC1A2; the disease is Alzheimer disease.