ABCA1 and Alzheimer disease: Interestingly, Yang et al. demonstrated that intracranial IL-17A overexpression increased ABCA1 protein levels in the hippocampus protein but not in cortex, decreased soluble Aβ levels in the hippocampus and cerebrospinal fluid, and improved glucose metabolism, suggesting that IL-17A may play a protective role in the pathogenesis of AD [173].