Additionally, CCH greatly enhanced the number of Aβ oligomer-positive/pTau cells, the expression of peroxidation products (4-HNE and 8-OHdG), mitochondrial fission proteins (Drp1 and Fis1), and decreased the expression of mitochondrial fusion proteins (Opa1 and Mfn1) in the CTX and thalamus (TH) of AD model mice at 12 month of age, demonstrating that CCH shifted the balance in mitochondrial morphology from fusion to fission [86]. This evidence concerns the gene MFN1 and Alzheimer disease.