It seems plausible that the association between the DAT1 VNTR and binge-eating behaviour indicates that dysregulation of dopamine reuptake may act as a common pathophysiologic mechanism in eating disorders with binge-eating behaviour and in disorders related to substance use.
These are the first two variants associated with the pathophysiology of ED in different populations and support a role for BDNF in the susceptibility to aberrant eating behaviors.
Comparison of 5-HTTLPR distribution in 195 female Japanese ED patients and 290 age- and gender-matched control subjects facilitated examining the association between the course of the disease and 5-HTTLPR in 138 of 195 ED subjects.
Various studies have evaluated the possible role of the -1438G/A polymorphism within the 5-HT2A receptor gene in the susceptibility to Eating Disorders (EDs).
Whereas previous investigations have suggested that the 5-HT (2C) receptor gene polymorphism is critically involved in the pathogenesis of affective and eating disorders, as yet the functional consequences being associated with the rare serine variant of the 5-HT (2C) receptor in humans are unclear.
These results support the involvement of BDNF in eating behaviour and further suggest its participation in the genetic susceptibility to ED, mainly ANR and low minBMI.
We investigated the genetic contribution of the BDNF-specific receptor neurotrophic tyrosine kinase receptor type 2 (NTRK2) to the susceptibility to ED.
Our data support a contribution of NTRK2 to the genetic susceptibility of ED, mainly ANP, and ED-related phenotypic traits, such as Harm avoidance and minBMI.
Providing confirmation that the BDNF gene is the true susceptibility gene for eating disorders could lead to rapid therapeutic progress in treating these disorders.
In addition, a more complete understanding of the signal transduction pathway via the p75 neurotrophin receptor (p75NTR) and TrkB receptors would provide new perspectives for treating eating disorders.
In addition, a more complete understanding of the signal transduction pathway via the p75 neurotrophin receptor (p75NTR) and TrkB receptors would provide new perspectives for treating eating disorders.
In addition, a more complete understanding of the signal transduction pathway via the p75 neurotrophin receptor (p75NTR) and TrkB receptors would provide new perspectives for treating eating disorders.
In addition, a more complete understanding of the signal transduction pathway via the p75 neurotrophin receptor (p75NTR) and TrkB receptors would provide new perspectives for treating eating disorders.
In addition, a more complete understanding of the signal transduction pathway via the p75 neurotrophin receptor (p75NTR) and TrkB receptors would provide new perspectives for treating eating disorders.
In addition, a more complete understanding of the signal transduction pathway via the p75 neurotrophin receptor (p75NTR) and TrkB receptors would provide new perspectives for treating eating disorders.
In addition, a more complete understanding of the signal transduction pathway via the p75 neurotrophin receptor (p75NTR) and TrkB receptors would provide new perspectives for treating eating disorders.
In addition, a more complete understanding of the signal transduction pathway via the p75 neurotrophin receptor (p75NTR) and TrkB receptors would provide new perspectives for treating eating disorders.
In addition, a more complete understanding of the signal transduction pathway via the p75 neurotrophin receptor (p75NTR) and TrkB receptors would provide new perspectives for treating eating disorders.
Our previous studies show that the brain-derived neurotrophic factor (BDNF) may play a role in the pathophysiology of major depressive disorders and eating disorders.
The current finding that the IGF2ApaI G polymorphism, which predisposes to weight gain, may also contribute to the pathology of eating disorders is intriguing.
In the present study, we examined the 171T/C polymorphism of the ghrelin receptor (growth hormone secretagogue receptor, GHSR) gene in patients diagnosed with EDs, because the subjects having ghrelin gene polymorphism (Leu72Met) was not detected in a Japanese population, previously.