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:Diabetes has been linked to an increased risk of mild cognitive impairment (MCI), a conditioncharacterized by a subtle cognitive decline that may precede the development of dementia. Theunderlying mechanisms connecting diabetes and MCI involve complex interactions between metabolicdysregulation, inflammation, and neurodegeneration. A critical mechanism implicated in diabetes andMCI is the activation of inflammatory pathways. Chronic low-grade inflammation, as observed in diabetes,can lead to the production of pro-inflammatory cytokines such as tumor necrosis factor-alpha(TNF-α), interleukin-6 (IL-6), interleukin-1 beta (IL-1β), and interferon-gamma (IFNγ), each of whichcan exacerbate neuroinflammation and contribute to cognitive decline. A crucial enzyme involved inregulating inflammation is ADAM17, a disintegrin, and metalloproteinase, which can cleave and releaseTNF-α from its membrane-bound precursor and cause it to become activated. These processes, inturn, activate additional inflammation-related pathways, such as AKT, NF-κB, NLP3, MAPK, andJAK-STAT pathways. Recent research has provided novel insights into the role of ADAM17 in diabetesand neurodegenerative diseases. ADAM17 is upregulated in both diabetes and Alzheimer's disease,suggesting a shared mechanism and implicating inflammation as a possible contributor to muchbroader forms of pathology and pointing to a possible link between inflammation and the emergenceof MCI. This review provides an overview of the different roles of ADAM17 in diabetes-associatedmild cognitive impairment diseases. It identifies mechanistic connections through which ADAM17and associated pathways may influence the emergence of mild cognitive impairment.