Herein, we have demonstrated that NHPs exhibiting SIB as adults have decreased DA function and display cognitive deficits as juveniles, both of these have also been seen in the context of human SIB.9, 10, 11, 15 We have also shown that treatment with guanfacine, an α2A agonist similar to one previously utilized to treat human SIB, was also effective in treating SIB in our cohort of macaques.24 The increased BPND found in SIB is likely related to the decreased intrasynaptic DA, which in turn may have been ameliorated by treatment with guanfacine. Here, IGKV2D-29 is linked to Cognitive impairment.