At physiologic nanomolar concentrations, S100B stimulates neurite outgrowth41 and exerts neuroprotective effects by preventing cell death and loss of mitochondrial function stemming from glucose deprivation.42 Conversely, at the pathologically elevated concentrations typical of the AD brain, S100B promotes AD pathology by processes including upregulation of the Aβ precursor protein43 and induction of apoptosis.44 The gene discussed is S100B; the disease is Alzheimer disease.