Kyoko Hasebe1, Laura Gray1, Chiara Bortolasci1, Bruna Panizzutti2, Mohammadreza Mohebbi3, Srisaiyini Kidnapillai1, Briana Spolding1, Ken Walder1, Michael Berk4, Gin Malhi5, Seetal Dodd3, Olivia M Dean4. 1. 1School of Medicine,Centre for Molecular and Medical Research,Deakin University,Geelong,Australia. 2. 4Laboratory of Molecular Psychiatry,Hospital de clínicas de Porto Alegre,Universidade Federal do Rio Grande do Sul,Porto Alegre,Brazil. 3. 5School of Medicine,IMPACT Strategic Research Centre,Deakin University,Geelong,Australia. 4. 2The Florey Institute of Neuroscience and Mental Health,Parkville,Australia. 5. 8Discipline of Psychiatry,Sydney Medical School,University of Sydney,Sydney,Australia.
Abstract
OBJECTIVE: This study aimed to explore effects of adjunctive N-acetylcysteine (NAC) treatment on inflammatory and neurogenesis markers in unipolar depression. METHODS: We embarked on a 12-week clinical trial of NAC (2000 mg/day compared with placebo) as an adjunctive treatment for unipolar depression. A follow-up visit was conducted 4 weeks following the completion of treatment. We collected serum samples at baseline and the end of the treatment phase (week 12) to determine changes in interleukin-6 (IL6), C-reactive protein (CRP) and brain-derived neurotrophic factor (BDNF) following NAC treatment. RESULTS:NAC treatment significantly improved depressive symptoms on the Montgomery-Asberg Depression Rating Scale (MADRS) over 16 weeks of the trial. Serum levels of IL6 were associated with reductions of MADRS scores independent of treatment response. However, we found no significant changes in IL6, CRP and BDNF levels following NAC treatment. CONCLUSION: Overall, this suggests that our results failed to support the hypothesis that IL6, CRP and BDNF are directly involved in the therapeutic mechanism of NAC in depression. IL6 may be a useful marker for future exploration of treatment response.
RCT Entities:
OBJECTIVE: This study aimed to explore effects of adjunctive N-acetylcysteine (NAC) treatment on inflammatory and neurogenesis markers in unipolar depression. METHODS: We embarked on a 12-week clinical trial of NAC (2000 mg/day compared with placebo) as an adjunctive treatment for unipolar depression. A follow-up visit was conducted 4 weeks following the completion of treatment. We collected serum samples at baseline and the end of the treatment phase (week 12) to determine changes in interleukin-6 (IL6), C-reactive protein (CRP) and brain-derived neurotrophic factor (BDNF) following NAC treatment. RESULTS:NAC treatment significantly improved depressive symptoms on the Montgomery-Asberg Depression Rating Scale (MADRS) over 16 weeks of the trial. Serum levels of IL6 were associated with reductions of MADRS scores independent of treatment response. However, we found no significant changes in IL6, CRP and BDNF levels following NAC treatment. CONCLUSION: Overall, this suggests that our results failed to support the hypothesis that IL6, CRP and BDNF are directly involved in the therapeutic mechanism of NAC in depression. IL6 may be a useful marker for future exploration of treatment response.