Notably, the role of PPARγ in cognitive and LTP performance has been identified in experimental models of neuronal seipin deficiency and aging (Zhou et al., 2016; d’Angelo et al., 2019), and PPARγ agonists have been reported to attenuate the βA peptide-dependent impairment of LTP (Costello et al., 2005). The gene discussed is BSCL2; the disease is hyperinsulinemic hypoglycemia, familial, 4.