These results suggested that alterations in glutamate metabolism in astrocytes of AD may be due to the abnormal expressions of GLUL and GLUD1. Additionally, M85 (aspartate_in→aspartate) flux, the metabolites (aspartate), and flux-related transporter (SLC1A3) were also significantly downregulated (Figures 2, 3A; Supplementary Tables S3, S4). Here, GLUL is linked to Alzheimer disease.