After 3 weeks of therapy, changing patterns of 18F-ML-10 uptake between baseline and ETA were visible. Acknowledgments This work was support by the US National Institutes of Health research grant U01 CA140230, as well as the UPCI shared resources award P30CA047904. The authors thank Aposense Ltd. for supplying the precursor for 18F-ML-10. The authors also thank the technology Inhibitors,research,lifescience,medical staff of the University of Pittsburgh
Medical Center PET-Cyclotron facility. Conflict of Interest None declared. Funding Information This work was support by the US National Institutes of Health research grant U01 “type”:”entrez-nucleotide”,”attrs”:”text”:”CA140230″,”term_id”:”35033013″,”term_text”:”CA140230″CA140230,
as well as the UPCI shared resources award P30CA047904.
Major depressive disorder (MDD) manifested in adolescence is common, recurrent, and often Inhibitors,research,lifescience,medical perpetuated into adulthood (Fombonne et al. 2001). MDD in adolescents frequently occurs in comorbidity with other psychiatric disorders and is an important contributor to increased risk of suicide, substance abuse, and behavioral problems (Harrington et al. 1994; Yorbik et al. 2004). Moreover, it disrupts occupational, social, emotional, and physical health and is frequently associated with poor psychosocial and academic outcome carrying Inhibitors,research,lifescience,medical considerable stigma (Fletcher 2008; Thapar et al. 2012). The etiology of MDD Inhibitors,research,lifescience,medical is considered complex and multifactorial, involving a purported interplay of multiple environmental and genetic factors (Kendler et al. 2013). In this regard, a miscellaneous set of distressful psychosocial events experienced early in life (e.g., maltreatment, neglect, abuse) has been consistently associated with an increased risk to manifest major depression (Kendler et al. 2000; Jaffee et al. 2002). On the other hand among the numerous
candidate genes evaluated with regard to MDD, those coding for the brain-derived neurotrophic factor (BDNF) and the serotonin transporter (SERT; 5HTT) have Inhibitors,research,lifescience,medical been particularly appealing for genetic association studies. Both molecules participate in cellular signaling systems that regulate the development and plasticity of neural circuits because involved in depression and anxiety (Martinowich and Lu 2008; Castrén and Rantamäki 2010); in addition a variety of cellular and molecular reciprocal interactions between BDNF with the serotonin (5HT) neural system exists (Martinowich and Lu 2008). In particular, two common genetic variants have been recurrently tested: the 44 pair base insertion/deletion polymorphism in the promoter region of the SLC6A4 gene (aka 5HTT-LPR), yielding long (L) or short (S) alleles; and the single-nucleotide polymorphism (A/G: rs6265) which predicts the substitution of valine to methionine at codon 66 in the prodomain of BDNF gene (Val66Met).