Apoptotic protein profiling demonstrated that CSA treatment significantly modulated key regulators of cell death in the AD/Si-GPR43 model, with the AD/Si-GPR43 + CSA group showing reduced BAX levels(2.46 ± 0.26 vs. AD/Si-GPR43: 3.58 ± 0.22; p < 0.05; Fig. 8C), while exhibiting increased BCL-2 expression (0.71 ± 0.11 vs. 0.48 ± 0.06; p < 0.05; Fig. 8D) and decreased Caspase-9 expression (1.16 ± 0.02 vs. AD/Si-GPR43: 1.39 ± 0.04; p < 0.05; Fig. 8E). Here, FFAR2 is linked to Alzheimer disease.