However, a recent study suggests that Fe65 may regulate transcription independent of AICD and has been implicated in long-term memory formation.23 Additionally, the expression of Fe65 in APP transgenic mice has shown decline in amyloid beta (Aβ) load,20,24 suggesting that targeting the interaction of Fe65/APP may provide a viable approach for treating AD. Here, APBB1 is linked to Alzheimer disease.