For instance, 11-month-old 3×Tg-AD mice showed a more significant decrease in SCFA than younger 3×Tg-AD mice, a pattern emerging later in wild-type mice.88 Additionally, AD-model Drosophila exhibited a notable reduction in acetate concentrations, alongside diminished Acetobacter and Lactobacillus populations.89 This evidence for the role of gut-microbial derived SCFA can be summarized into an understanding that SCFA can have a role in protecting AD-related histopathology, specifically phosphorylated Tau, in the early stages of AD mice models. This evidence concerns the gene MAPT and Alzheimer disease.