The results showed that in the HFD brains, various genes involved in the processing of Amiloid β Precusor (APP) and TAU (Aplp1, Aplp2, App, Apba3, Apbb2, Apoe, Ckk5, Clu, Ctsl, Mapt, Prkca, Prkce and Hsd17b10), in synaptic function (Ache), in AD-related iperphosphorylation (Gsk3α, GCdk5 and Prkca), and in inflammation (MPO and Il-1α) (Table 1) were upregulated in comparison with lean brains. This evidence concerns the gene CTSL and Alzheimer disease.