Molecular interactions of diabetes medications with alzheimer's related targets by molecular docking
Abstract
Diabetes, a prevalent chronic disease known for its complications such as cardiovascular issues, eye damage, and neuropathy, has increasingly been linked to an elevated risk of Alzheimer's disease and cognitive impairment. Individuals with diabetes are approximately twice as likely to experience cognitive dysfunction compared to the general population. This heightened risk is potentially mediated by factors such as hypoglycemic episodes, which can negatively impact brain function, particularly the hippocampus, a key region for memory. Furthermore, shared molecular and cellular characteristics between diabetes and Alzheimer's, such as the role of insulin in amyloid plaque formation, suggest a direct link between insulin resistance in the brain and the development of Alzheimer's-related pathology. This study investigates the potential of two commonly prescribed diabetes medications, Ertugliflozin and Sitagliptin, to impact Alzheimer's disease-related factors. Ertugliflozin, an SGLT2 inhibitor, lowers blood glucose by increasing glucose excretion via the kidneys, while Sitagliptin, a DPP-4 inhibitor, enhances insulin secretion and reduces glucagon secretion by preventing the breakdown of incretin hormones. Molecular docking was performed to assess the interaction of these drugs with five key targets implicated in Alzheimer's disease: amyloid-β, β-secretase (BACE1), γ-secretase, and acetylcholinesterase (AChE). The aim was to determine whether Ertugliflozin and Sitagliptin…
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