CUTA (cutA divalent cation tolerance homolog) is a ubiquitously expressed protein with emerging roles in metal homeostasis and disease pathogenesis. Primary function: CUTA participates in copper and divalent cation regulation, with evidence suggesting involvement in acetylcholinesterase anchoring at neuronal membranes 1. Mechanism: CUTA localizes primarily to mitochondria and forms trimeric oligomers 1. In Alzheimer's disease pathogenesis, CUTA interacts with β-secretase (BACE1) to inhibit amyloid-β (Aβ) generation from APP processing, while reciprocally modulating intracellular copper levels 2. Disease relevance: CUTA dysregulation associates with multiple conditions: (1) Alzheimer's disease, where reduced CUTA and copper levels occur in affected brain tissue 2; (2) depression, where CUTA expression changes through altered methylation influence disease susceptibility 3; and (3) autoimmune thyroid disease, showing differential DNA methylation between Graves and Hashimoto diseases 4. Clinical significance: CUTA represents a potential therapeutic target for neurodegenerative and psychiatric disorders. The protein's copper-binding properties enable its application in nanomedicine platforms for treating infections and inflammatory conditions 56. Further investigation is needed to fully elucidate CUTA's physiological roles beyond metal homeostasis.