A large number of central nervous system impairments occur in subjects with chronic HCV infection regardless of liver disease. Brain-derived neurotrophic factor (BDNF) plays an essential role in the adult brain concerning its development and proper functioning. Our study aimed at contributing to the discussion on the involvement of BDNF in neurocognitive disorders associated with HCV infection.
We aimed to evaluate the prevalence of neurocognitive disorders in a cohort of HCV-infected subjects, to measure serum BDNF levels in the same cohort according to the degree of neurocognitive disorders, and to evaluate serum BDNF level modification in HCV-infected patients after direct antiviral agents (DAA) therapy.
We enrolled patients scheduled for DAA therapy in January 2018 from three infectious disease units in Eastern Sicily. Each participant was evaluated for neurocognitive status with MoCA score at baseline and 12 and 24 weeks after the end of therapy. Moreover, we measured serum BDNF levels at baseline and 12 weeks after the end of therapy.
Of 70 HCV-infected patients, 42 (60%) were males. The average age was 57 ± 19 years and the average ALT level was 79 ± 24 UI/mL; 38 (54.3%) individuals had HCV genotype 1 infection and 23 (32.8%) and 25 (35.7%) individuals had F1 and F2 fibrosis stages, respectively. Moreover, 67 (95.7%) individuals achieved sustained virological response. The MoCA score at baseline identified four groups of patients. Higher MoCA scores 24 weeks after the end of therapy highlighted the improvement of neurocognitive status in all groups. Serum BDNF levels in the same four groups, measured 12 weeks after the end of DAA therapy, appeared significantly modified compared to baseline serum BDNF levels, matching the improvement of MoCA score results obtained 24 weeks after DAA therapy.
The serum BDNF level may represent a useful marker of cognitive dysfunction in patients with HCV infection and a useful index for assessing the post-therapy follow-up.
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