AD involves a combination of processes, including decreased acetylcholinesterase levels, reduced insulin sensitivity, the accumulation of advanced glycation end-products (AGEs), the dysfunction of APOE, etc. Hence, it is of utmost importance to develop an animal model of Late-Onset Alzheimer’s Disease (LOAD) that accurately replicates the pathology observed in humans. This evidence concerns the gene INS and early-onset autosomal dominant Alzheimer disease.