By preventing reactive astrocytes from producing gamma-aminobutyric acid (GABA), selegiline has been shown to enhance synaptic plasticity, learning, and memory in AD mice.55 It has also been suggested that MAO-A inhibitor also offers neuroprotection.9 Our docking studies also showed that pillion (-9.9 kcal/mol) has more affinity towards MAO-A compared to the native ligand as well as the control drug selegiline (-7.4 kcal/mol). Here, MAOA is linked to Alzheimer disease.