BACE1 cleaves multiple substrates including NRG1, which is required for ErbB4-mediated PV interneuron maintenance. Full BACE1 inhibition has failed clinically, partly due to mechanism-based toxicities (BACE1 substrate effects). Sub-therapeutic APP cleavage inhibition might selectively rescue NRG1-ErbB4 signaling to PV cells while leaving Aβ generation largely intact — a paradoxically useful property if E/I imbalance is the primary driver of cognitive symptoms. Falsifiable prediction: BACE1 inhibitor NB-360 at 0.3× IC50 (APP substrate) in 5xFAD mice should increase PV interneuron NRG1-ErbB4 signaling (pErbB4/ErbB4 ratio) by ≥50%, restore gamma oscillation peak power by ≥35%, and improve novel object recognition index by ≥20%, without reducing Aβ42 by >10% in cortex. The selective NRG1 restoration mechanism must be confirmed by NRG1 type III ELISA.