Indeed, in Alzheimer's disease, increasing plaque complexity (diffuse to diffuse neuritic to dense-core neuritic) is associated with more βAPP-immunoreactive neurites and more activated astrocytes overexpressing S100B (Mrak et al., 1996), which could further exacerbate neuronal transport deficits, through its promotion of βAPP synthesis and neurite outgrowth and its dose-dependent induction of microtubule associated protein 2 (Li et al., 1998). Here, S100B is linked to early-onset autosomal dominant Alzheimer disease.