International journal of psychiatry in clinical practice · 2014
BDNF and Artemin are increased in drug-naïve non-depressed GAD patients: preliminary data.
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Pallanti Stefano, Tofani Tommaso, Zanardelli Matteo, Di Cesare Mannelli Lorenzo, Ghelardini Carla
Аннотация
OBJECTIVE: While the role of neuronal and glial plasticity are well established in the pathophysiology of mood disorders, the pattern and measures of neuronal and glial cell line-derived neurotrophic factors are unknown in generalized anxiety disorder (GAD). The present study evaluates brain-derived neurotrophic factor (BDNF) and Artemin (ARTN) plasma levels in GAD patients.
METHODS: Fourteen drug-naïve GAD patients without major depression were enrolled and plasmatic levels of BDNF and ARTN mRNA were measured by RT-PCR, and compared to matched healthy controls.
RESULTS: The results showed an unexpected increase in mRNA levels of both BDNF and ARTN in patients with GAD, that appeared almost doubled when compared to healthy controls. In comparison, both BDNF and ARTN are reduced in patients with major depressive disorder. Further, the results are intriguing and might involve distinguishing pathophysiological pathways.
CONCLUSIONS: This is the first report of increased levels of a neurotrophic factor and of a glial cell line-derived neurotrophic factor family member in GAD patients. While further studies to confirm these results and the functional meaning in terms of pathophysiology of GAD are needed, the potential conceptual and clinical meanings are discussed.
METHODS: Fourteen drug-naïve GAD patients without major depression were enrolled and plasmatic levels of BDNF and ARTN mRNA were measured by RT-PCR, and compared to matched healthy controls.
RESULTS: The results showed an unexpected increase in mRNA levels of both BDNF and ARTN in patients with GAD, that appeared almost doubled when compared to healthy controls. In comparison, both BDNF and ARTN are reduced in patients with major depressive disorder. Further, the results are intriguing and might involve distinguishing pathophysiological pathways.
CONCLUSIONS: This is the first report of increased levels of a neurotrophic factor and of a glial cell line-derived neurotrophic factor family member in GAD patients. While further studies to confirm these results and the functional meaning in terms of pathophysiology of GAD are needed, the potential conceptual and clinical meanings are discussed.