Conversely, inhibition of PKCι and the closely related PKCζ by the prostate apoptosis-response 4 (PAR-4) protein has been recently shown to increase proteolytic processing of amyloid precursor protein [56], [57] and to exacerbate Aβ accumulation and toxicity in mouse models of Alzheimer's disease [58], [59] suggesting a role for PKCι in modulating survival. Here, APP is linked to early-onset autosomal dominant Alzheimer disease.