The steady increase in average lifespan of humans and animals has made the problem of aging-related cognitive impairment a significant issue. Alzheimer's disease (AD) in humans is a degenerative brain disease characterized by the loss of basic body functions due to neuronal damage, and canine cognitive dysfunction observed in dogs is stated to resemble human AD. Acetylcholine esterase (AChE) plays a role in the pathogenesis of the disease, and its inhibition prevents AChE-induced Aβ aggregation. Other pathological factors, including oxidative stress, inflammation and the Wnt pathway, also contribute to AD pathogenesis. The use of AChE inhibitor (AChEI) is the most effective way among the several available options for improving cholinergic symptoms. Although acotiamide is an AChEI, there is currently no information regarding its use in AD; therefore, this study aimed to examine the effects of acotiamide in an AD model for the first time. A total of 26 mice were divided into 4 groups: control, sham, Alzheimer and Alzheimer+Acotiamide. To create an experimental AD model, streptozotocin was administered intracerebroventricularly. In addition, acotiamide was administered intraperitoneally to the animals in the Alzheimer+Acotiamide group. The study evaluated AChE, choline acetyltransferase, β-secretase (BACE1), tumor necrosis factor-alpha, interleukin-10, α7nicotinic acetylcholine receptor, glycogen synthase kinase3beta, 8-hydroxy-2-deoxyguanosine and glutathione parameters; along with the number of neurons in the CA1 and CA3 regions, and the thickness in these areas. It can be concluded from results that acotiamide could prevent neuroinflammation, reduce AChE and BACE1 protein levels and may be effective in the treatment/prevention of AD.