Multiple intracellular mechanisms, including activation of α-secretases and Aβ-degrading enzyme, production of neurotrophins, increase of neuronal glucose uptake, upregulation of NF-κB, PI3K-Akt, MAPK, Jak-STAT, ERK1/2 phosphorylation and downregulation of caspase-3, inhibition of endoplasmic reticulum stress and autophagy, modulation of LTP and potassium channel activity, appear to be involved in neuropeptide-induced neuroprotection in Alzheimer's disease. Here, SOAT1 is linked to early-onset autosomal dominant Alzheimer disease.