Hepatitis C infection caused by the hepatitis C virus (HCV) presents a global health challenge, affecting approximately 71 million individuals worldwide and leading to significant liver-related morbidity and mortality. Despite advancements in therapy, chronic HCV infection often progresses to liver carcinoma and cirrhosis, necessitating liver transplantation. Beyond hepatic manifestations, patients with HCV frequently experience neuropsychiatric symptoms, including anxiety, fatigue, depression, and cognitive impairment, which can adversely impact their quality of life and treatment outcomes. Importantly, cognitive deficits in HCV patients are not solely attributable to liver dysfunction, suggesting a direct role of the virus in cerebral dysfunction. Neurocognitive impairment, affecting attention, memory, processing speed, and executive function, is prevalent in up to half of HCV-infected individuals, irrespective of liver disease severity. Mechanisms underlying cognitive changes in HCV involve neuroinvasion and direct viral damage, with evidence of HCV replication and distinct viral populations in the central nervous system (CNS). Additionally, HCV-induced cryoglobulinemia can precipitate vasculitis, exacerbating neurological complications. Understanding these pathogenic mechanisms is crucial for developing targeted interventions to mitigate cognitive impairment in HCV patients. This narrative review provides insights into the complex interplay between HCV infection and cognitive dysfunction, emphasizing the need for comprehensive evaluation and management of neuropsychiatric symptoms in hepatitis C care.