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Diabetes patients have reduced basal cognitive abilities like learning, memory, and perceptual quickness, as well as a 65 percent higher risk of acquiring AD. AD and diabetes share a number of risk factors, including elevated cholesterol, Aβ deposition, degeneration, inflammation, oxidative stress, cardiovascular diseases, dysmetabolism syndrome, τ-protein phosphorylation, glycogen synthesis kinase 3, apoptosis and apolipoprotein E4. This study explores the potential inhibitory effects of imatinib at doses of 1 and 5 mg/kg, with a particular emphasis on the role of c-Abl in amyloidogenesis, a common mechanism that underlies T2DM and AD. Induction of T2DM induced AD by HFD-STZ-Aβ_25-35 model. Assessment of behavioural parameters like polydipsia, polyphagia, morris water maze & passive avoidance test; biochemical estimation of glucose, insulin, oxidative stress (SOD, GSH, Cat, TBARS), neuroinflammation (IL-1β, IL-6, TNF-α, NF-κβ), Aβ levels, c-Abl through ELISA technique. Imatinib (1 & 5 mg/kg) results in a reduction in food and water intake, as well as a reduction in memory impairment in the Morris water maze and passive avoidance test. Further, it normalises glucose, insulin, and anti-oxidant elements (SOD, GSH, Cat) levels, while decreasing TBARS levels. Additionally, ELISA data demonstrated a reduction in neuroinflammation (downregulation of IL-1β, IL-6, TNF-α, and NF-κβ), Aβ accumulation, and c-Abl levels by imatinib (1 & 5 mg/kg). Consequently, c-Abl can play a crucial role in the mediation of amyloidogenesis induced by T2DM, thereby establishing a connection between T2DM and AD. Therefore, Imatinib has the potential to treat and prevent the progression of T2DM to AD.