Consistent with previous reports, in both in vivo and in vitro models of AD, a compromised ANLS was found, and FGF21 delivered centrally or peripherally alleviated AD-related degeneration in mice; blocking FGFR1, however, prevented the beneficial effects induced by FGF21, including the alleviation of tau pathology and the upregulation of ATP, MCT2, and MCT4 in the brain [105]. Here, FGF21 is linked to Alzheimer disease.