Contents lists available at ScienceDirect Neurology, Psychiatry and Brain Research journal homepage: www.elsevier.com/locate/npbr An 8 week prospective study on the relationship between major depressive episode and serum brain derived neurotrophic factor in a Nigerian tertiary hospital Frances N. Adiukwu a, ⁎ , Princewill C. Stanley b , Jude U. Ohaeri c a Department of Neuropsychiatry, University of Port Harcourt Teaching Hospital, Rivers State, Nigeria b Department of Psychiatry, Faculty of Clinical Sciences, University of Port Harcourt, Rivers State, Nigeria c Department of Psychological Medicine, University of Nigeria, Nsukka, Enugu, Nigeria ARTICLE INFO Keywords: Major depressive episode Pathophysiology Brain derived neurotrophic factor Neurobiology Depression Nigeria ABSTRACT Background: Current views on the etiology of Major Depressive Diorder(MDD) emphasizes environmental and biological interplay. Recent studies have implicated reduction in Brain Derived Neurotrophic Factor (BDNF) in the pathophysiology and as a biomarker of major depression (Neurotrophin Hypothesis of Depression). This study aimed at showing that the Neurotrophin hypothesis of depression is relevant in the pathophysiology of Major Depressive Episode in Southern Nigeria. Methods: Consecutive consenting patients diagnosed with Major Depressive Episode (MDE) using the Structured Clinical Interview for DSM (SCID) and age and sex matched controls were enrolled into this study. Serum BDNF was measured prior to commencement of treatment as baseline and 8 weeks after treatment. Depression severity was rated with the Hamilton Depression Rating Scale (HAM-D) and Patient Health Questionnaire (PHQ-9). Results: Seventy-five cases and 75 age and sex matched controls were recruited. The mean ± SD of serum BDNF of depressed patients (26.09 ng/ml ± 1.96) was significantly lower than those of age and sex matched controls (28.13 ng/ml ± 1.47) P < 0.01. The study had a follow up rate of 48% after 8 weeks of treatment. Serum BDNF post treatment was significantly higher than baseline. Limitations: This was a single center study with a high drop-out rate. Conclusion: The result of this study adds to the mounting evidence in support of the neurotrophin hypothesis of depression. 1. Introduction Depression is a highly prevalent disorder affecting over 120 million of the world’s population (Lépine & Briley, 2011). It is one of the leading causes of disability worldwide and is estimated to be the 2nd cause of disability worldwide by 2020. It is associated with increased morbidity, mortality, suicide rate and cognitive impairment (Ojagbemi, Oladeji, Abiona, & Gureje, 2013). Prevalence rates globally are highly variable ranging from 1.5%–19% (Weissman et al., 1996). In Nigeria, the point prevalence of Major Depressive Episode (MDE) ranges be- tween 3.1%–5.2% (Amoran, Lawoyin, & Lasebikan, 2007; Gureje, Uwakwe, Oladeji, Makanjuola, & Esan, 2010). Brain Derived Neurotrophic Factor (BDNF) is a member of the neurotrophin (NT) family along with Nerve Growth Factor (NGF), Neurotrophin 3 (NT3) and neurotrophin 4 (NT4) found in the mam- malian brain. It was first purified in 1982 where its function was thought to promote cell survival (Adachi, 2014; Barde, Edgar, & Thoenen, 1982; Dwivedi, 2013). The neurotrophin family of which BDNF is a member is important in the regulation of cell survival and cell differentiation during development (Bramham & Messaoudi, 2005). BDNF has emerged as a crucial mediator in neuronal plasticity and also has a positive impact on neurogenesis in the adult brain (Calabrese et al., 2014). The neurotrophic hypothesis of depression proposes that depression is associated with reduced brain BDNF levels and that antidepressant treatments alleviate depressive behaviour and increase BDNF levels (Duman & Li, 2012; Lee & Kim, 2010). This hypothesis postulates that a reduction in BDNF plays a direct role in the pathophysiology of de- pression and that Major depression is associated with impaired neu- ronal plasticity. Antidepressant treatment promotes several forms of neuronal plasticity such as neurogenesis, synaptogenesis neuronal ma- turation and increases BDNF activity. Karege et al. demonstrated that https://doi.org/10.1016/j.npbr.2019.03.007 Received 10 December 2018; Received in revised form 13 March 2019; Accepted 22 March 2019 ⁎ Corresponding author at: Department of Neuropsychiatry, University of Port Harcourt Teaching Hospital, P.M.B 6173, Port Harcourt, Rivers State, Nigeria. E-mail address: francesadiukwu@gmail.com (F.N. Adiukwu). Neurology, Psychiatry and Brain Research 32 (2019) 42–47 0941-9500/ © 2019 Elsevier GmbH. All rights reserved. T