In studies on the amyloid precursor, protein/presenilin 1 (APP/PS1) mouse model of AD, these researchers found that selegiline reduced the aberrant levels of GABA initially by inhibiting MAO-B but that increased activity of the compensatory GABA-synthesizing enzyme diamine oxidase after longer administration of selegiline resulted in increased levels of GABA again; they found that a highly selective, reversible MAO-B inhibitor (KDS2010) did not have this effect and reversed learning and memory impairment in this mouse model (Park et al 2019). The gene discussed is MAOB; the disease is Alzheimer disease.