IGF1 and Alzheimer disease: Protein restriction with supplementation of nonessential amino acids reduced IGF-I concentrations in male 3xTg-AD mice displaying significant cognitive impairment and Alzheimer disease–like pathology, which resulted in a decrease in tau phosphorylation in the hippocampus, but without affecting the concentrations of β-amyloid, and alleviation of the age-dependent impairment in cognitive performance (34).