In T2D, the enzyme Beta-Secretase 1, which plays a key role in the production of amyloid-beta (Aβ) in Alzheimer’s disease, also contributes to metabolic dysfunction; BACE1 activation leads to increased neuroinflammation and impaired insulin signaling, while simultaneously promoting the accumulation of protein tyrosine phosphatase 1B which disrupts insulin signaling and exacerbates glucose homeostasis dysfunction, further linking metabolic dysregulation with neurodegenerative processes. This evidence concerns the gene INS and early-onset autosomal dominant Alzheimer disease.