CNTN3 (contactin 3) is a cell adhesion molecule that mediates cell surface interactions during nervous system development and has neurite outgrowth-promoting activity 1. The protein functions through its extracellular domains, with the second Fibronectin domain (Fn2) mediating binding to the Amyloid Precursor Protein (APP), specifically to APP's copper binding domain 2. CNTN3 expression is developmentally regulated, peaking around birth and during infancy before declining in the adult brain 3. The protein shows differential expression patterns across various disease contexts. In tuberous sclerosis complex (TSC), CNTN3 is significantly down-regulated in cortical tubers during early postnatal development, which may contribute to neuropsychiatric comorbidities 3. In dementia, CNTN3 levels in cerebrospinal fluid are reduced in Parkinson's disease dementia/dementia with Lewy bodies compared to Alzheimer's disease, suggesting distinct alterations across neurodegenerative conditions 4. CNTN3 also shows dysregulation in various cancers, including colorectal cancer where it may serve as a diagnostic biomarker 5, and glioblastoma where it is underexpressed compared to lower-grade astrocytic tumors 6. The protein is subject to microRNA regulation, with miR-3675b directly targeting CNTN3's 3'-UTR 7.