Furthermore, we observed that BACE1 levels increase in dystrophic presynaptic terminals that are in close proximity to amyloid plaques in AD and APP transgenic brains [24], [26] and that fibrillar and oligomeric Aβ42 cause BACE1 levels to increase ∼1.5–3-fold in primary neuron cultures [25]. Here, APP is linked to Alzheimer disease.