ABCA1 and Alzheimer disease: A previous study has reported that there is an accumulation of Th17 cells in the brain parenchyma of AD mice, and the secreted cytokine IL-17 is found to accumulate around Aβ plaques; furthermore, overexpression of IL-17 can significantly promote the expression of ABCA1 in vascular endothelium, accelerate the transport of Aβ from the brain parenchyma to the circulatory system, and reduce CAA lesions in the process of AD[111].