Pulmonary rehabilitation and BDNF levels in patients with chronic obstructive pulmonary disease: A pilot study.

BACKGROUND: COPD physiopathology involves multiple pathways and evidence indicates that brain-derived neurotrophic factor (BDNF) is an important biomarker associated with parameters of COPD severity. This study aimed to analyze the time course of the effects of a pulmonary rehabilitation program (PRP) on BDNF levels and on functional status in COPD patients. METHODS: Patients were enrolled in a 24-session PRP. Exercise capacity, dyspnea, health-related quality of life, and the BODE index were assessed at baseline and after the PRP. BDNF plasma levels were measured at baseline (immediately before the 1st session), after the 1st session, and before and after the 24th session. RESULTS: Sixteen patients were included. A reduction in BDNF levels was observed after the 1st session and an increase was observed between the end of the 1st session and the beginning of the 24th session. The PRP promoted an improvement in exercise capacity and health-related quality of life and a reduction in dyspnea and the BODE index. CONCLUSION: Exercise acutely reduced BDNF levels, an effect that was nullified by the overall intervention.

The modulation of inflammatory parameters, Brain-derived neurotrophic factor levels and global histone H4 acetylation status in peripheral blood of patients with Gaucher disease type 1.

OBJECTIVES: Gaucher's disease type 1 (GD1) pathophysiology includes an imbalance on brain-derived neurotrophic factor (BDNF) levels and in the inflammatory system. However, the pathways involved remain poorly understood. The hypothesis of this study is that epigenetic mechanisms might be involved, at least partially, in this phenomenon. DESIGN AND METHODS: This study investigated the BDNF modulation, global histone H4 acetylation and pro- and anti-inflammatory cytokines levels in the peripheral blood of GD1 patients (n=10) when compared with control samples (CS) (n=11). RESULTS: The results showed a significant increase in Chitotriosidase (CT) (p=0.019) and decreased ß-glucosidase (GBA) activities (p=0.001) in GD1 samples when compared to CS, for GD1 diagnostic confirmation. Reduced levels of BDNF (p=0.004) and elevated levels of TNF-α (p=0.017) and IL-4 (p=0.035) were also found in the GD group. No significant differences were observed in IL-6 or IL-17a levels between groups (p>0.05). Finally, a trend on higher global histone H4 acetylation levels (p=0.054) was observed in the control group when compared to GD1 individuals. CONCLUSIONS: Combined, these results suggest inflammatory cytokines imbalance, reduced BDNF levels and global histone H4 hypoacetylation status in GD type 1 physiopathology. These preliminary findings may open new avenues to introduce therapies and strategies in the preventive management and treatment of this population.