The hypothesis that hyperactive behavior observed in different models of amyloidosis is due to an alteration in GABAergic synapses is supported by the fact that mice lacking the GABA transporter subtype 1 (GAT1), responsible for the reuptake of GABA after its release, exhibit a hyperactive phenotype (Chen et al., 2015), and that mice lacking GAD67, the enzyme that catalyzes the decarboxylation of glutamate to synthesize GABA, also show a hyperactive phenotype (Smith, 2018). Here, SLC6A1 is linked to amyloidosis.