Plasma Brain-derived Neurotrophic Factor Levels Research Articles

394 – Implication of genetic polymorphisms and changes in expression levels of proteins regulating neuronal plasticity and apoptosis in schizophrenia disorder

Introduction Pathologic changes in neuronal plasticity and apoptosis are important factors influencing alterations in synaptic transmission and impaired cognitive function, characteristic features of schizophrenia. Brain derived neurotrophic factor (BDNF), complexin-2, and annexin A-5 are known as members of regulatory pathways responsible for maintenance of neuronal plasticity and apoptosis. Objectives The study was focused on assessment of possible association of functional single nucleotide polymorphisms (SNPs) and expression levels of BDNF, complexin-2, and annexin A-5 with schizophrenia. Aims For this purpose we investigated functional polymorphisms and plasma levels of these proteins in schizophreniaaffected neuroleptic-treated and neuroleptic-free patients and healthy controls. Methods DNA samples were genotyped by polymerase chain reaction with sequence-specific primers. Plasma levels of BDNF, complexin-2, and annexin A-5 were measured with an enzyme-linked immunosorbent assay. The significance of differences between allele and phenotype frequencies in study groups was determined using Pearson's χ2 test. For evaluation of intergroup differences in the levels of BDNF, complexin-2, and annexin A-5, both parametric and non-parametric statistics were used. The assessment of correlation between the measured parameters within each group was also performed. P-values less than 0.05 were considered significant. Results In patients with schizophrenia, as compared to controls, the carriers of mutant alleles of the functional polymorphisms of BDNF, complexin-2, and annexin A-5 genes were overrepresented, and the blood levels of these proteins were altered. Conclusions Functional polymorphisms of genes encoding BDNF, complexin-2, and annexin A-5 proteins are associated with schizophrenia resulting in altered expression levels of these proteins upon this disorder.

785 – Attributional retraining group therapy versus selective serotonin reuptake inhibitors: neurobiological effects

Objective The aim of this study was to compare the effectiveness of attribution retraining group therapy (ARGT) versus selective serotonin reuptake inhibitors (SSRI) in the treatment of major depressive disorder (MDD), generalized anxiety disorder (GAD) and obsessive-compulsive disorder (OCD). Methods 109 patients with MDD, GAD and OCD were recruited from the outpatient department of a tertiary referral hospital between 2007 and 2008. Subjects were sequentially recruited and randomized into ARGT group (n=63) and SSRI group (n=66) for an 8-week treatment period. 54 outpatients in ARGT group and 55 outpatients in SSRI group completed the study. All subjects were assessed using Hamilton Depression Scale, Hamilton Anxiety Scale before and after treatment. Yale-Brown Obsessive Compulsive Scale was employed only for OCD subjects. Plasma hormone levels of serotonin, norepinephrine, cortisol, adrenocorticotropic hormone, and brain-derived neurotrophic factor (BDNF) were measured at baseline and at 8 weeks. Results Symptom scores were reduced significantly in both ARGT and SSRI treatment groups (p Conclusions Our findings suggest that ARGT may modulate plasma cortisol levels and take effect to the HPA axis as opposed to SSRIs which may up-regulate plasma serotonin and BDNF levels via a different pathway to produce an overall improvement in the clinical condition of patients.

Alcohol, Brain Derived Neurotrophic Factor and Obesity among People Living with HIV.

IntroductionIn an expanding HAART era, obesity has become a health problem among persons living with HIV (PLWH). Whereas the rising level of obesity has been largely attributed to poor nutrition and exercise habits, differences in biological factors may explain why some individuals gain more weight than others. Thus, our main goal is to prospectively determine in PLWH whether plasma brain-derived neurotrophic factor (BDNF), and hazardous alcohol use (HAU), two overlooked but highly prevalent conditions among PLWH, correlate with an adverse anthropometric profile. Also to test whether these relationships varied in men and womenMethodsThe Platelets mediating Alcohol and HIV Damage Study (PADS) is an ongoing multiethnic study of 400 PLWH receiving regular medical care in South Florida (37% females and 63% males). Semi-annual visits consisted of a medical exam, including anthropometrics to assess both general (body mass index: BMI) and central obesity (waist and hip circumferences). Participants also completed health history questionnaires, and provided a fasting blood sample to obtain BDNF and immune and biochemical assessments.ResultsA sizable proportion of participants met the National Institutes of Health definition of overweight (BMI = 25–29.9 kg/m2; 26%) and obese (BMI ≥ 30 kg/m2; 35%). Women were more likely to be obese than men (OR=4.9, 95% CI=2.9–8.2, p=0.0001). Compared to men, women also exhibited the highest mean plasma BDNF levels (9,959 ± 6,578 vs. 7,470 ± 6,068 pg/ml, p=0.0001). Additional analyses indicated that HAU, particularly heavy drinkers, had the smallest waist and hip circumferences if they were males, but the opposite if they were females. High BDNF levels were positively correlated with BMI. Linear regression analysis revealed that gender, BDNF, and HAU were the best predictors of BMI.ConclusionIn summary, our findings offer novel insights into the relationships between BDNF, and alcohol use among overweight and obese PLWH. Our results also suggest that these relationships may be inherently different by gender.

Plasma brain-derived neurotrophic factor level may contribute to the therapeutic response to eye movement desensitisation and reprocessing in complex post-traumatic stress disorder: a pilot study.

Plasma brain-derived neurotrophic factor level may contribute to the therapeutic response to eye movement desensitisation and reprocessing in complex post-traumatic stress disorder: a pilot study - Volume 24 Issue 6

Changes in plasma and cerebrospinal fluid biomarkers in aged patients with early postoperative cognitive dysfunction following total hip-replacement surgery

We hypothesized that different patterns of biomarkers of brain injury and inflammation exist in aged patients with postoperative cognitive dysfunction (POCD) after total hip-replacement with spinal anesthesia. Eighty-three patients older than 65years undergoing elective total hip-replacement surgery were enrolled in this prospective observational study. The CSF levels of Tau, phosphorylated-tau (pTau), amyloidβ1-42 (Aβ1-42), Tau/Aβ1-42, pTau/Aβ1-42, BDNF, IL-6, and IL-1β were measured preoperatively. Perioperative plasma levels of IL-1β, IL-6, brain-derived neurotrophic factor (BDNF), C-reactive protein (CRP), and malonaldehyde (MDA) as well as neurocognitive tests were determined preoperatively and sevendays postoperatively. Sixty-one patients completed both the CSF and blood samples collection and the neurocognitive tests. POCD occurred in 24.6% of patients at sevendays after surgery. Patients with POCD had significantly higher IL-1β, Tau/Aβ1-42, pTau/Aβ1-42, and a lower level of Aβ1-42 in CSF when compared with the Non-POCD group (P<0.05). Furthermore, POCD patients displayed significantly higher plasma levels of MDA when compared with Non-POCD patients at sevendays after surgery (P<0.05). There was no difference in preoperative CSF levels of Tau, IL-6, and pTau as well as plasma levels of IL-1β, IL-6, BDNF and CRP between POCD and Non-POCD groups (P>0.05). The POCD patients were associated with higher postoperative plasma levels of MDA, and higher IL-1β and lower Aβ1-42 levels in preoperative CSF that might predispose the development of POCD in aged patients following total hip-replacement surgery with spinal anesthesia.

BDNF Val 66 Met and 5-HTTLPR genotype moderate the impact of early psychosocial adversity on plasma brain-derived neurotrophic factor and depressive symptoms: A prospective study

Recent studies have emphasized an important role for neurotrophins, such as brain-derived neurotrophic factor (BDNF), in regulating the plasticity of neural circuits involved in the pathophysiology of stress-related diseases. The aim of the present study was to examine the interplay of the BDNF Val66Met and the serotonin transporter promoter (5-HTTLPR) polymorphisms in moderating the impact of early-life adversity on BDNF plasma concentration and depressive symptoms. Participants were taken from an epidemiological cohort study following the long-term outcome of early risk factors from birth into young adulthood. In 259 individuals (119 males, 140 females), genotyped for the BDNF Val66Met and the 5-HTTLPR polymorphisms, plasma BDNF was assessed at the age of 19 years. In addition, participants completed the Beck Depression Inventory (BDI). Early adversity was determined according to a family adversity index assessed at 3 months of age. Results indicated that individuals homozygous for both the BDNF Val and the 5-HTTLPR L allele showed significantly reduced BDNF levels following exposure to high adversity. In contrast, BDNF levels appeared to be unaffected by early psychosocial adversity in carriers of the BDNF Met or the 5-HTTLPR S allele. While the former group appeared to be most susceptible to depressive symptoms, the impact of early adversity was less pronounced in the latter group. This is the first preliminary evidence indicating that early-life adverse experiences may have lasting sequelae for plasma BDNF levels in humans, highlighting that the susceptibility to this effect is moderated by BDNF Val66Met and 5-HTTLPR genotype.

278 Interleukin and Neurotrophic Factor Plasma Expression are Related to Disease Severity in Children with Influenza A (H1N1) Virus Infection

Background and AimsIn the last years the world has been facing a new pandemic caused by a H1N1 influenza virus, showing particular virulence in children. Cytokines and neurotrophic factors seem...

Decreased plasma levels of brain-derived neurotrophic factor and its relationship with obesity and birth weight in obese Japanese children

Brain-derived neurotrophic factor (BDNF) plays important roles in the central regulation of food intake and body weight control. However, little is known about the role of BDNF in childhood obesity. To investigate the relationship between plasma levels of BDNF and anthropometric factors, metabolic derangements due to obesity, adipocytokine levels and birth weight in obese Japanese children. Sixty-six obese Japanese children aged from 5 to 15 years old were enrolled. The age-matched control group consisted of 32 non-obese healthy children. The plasma levels of BDNF and adipocytokines (leptin and adiponectin) were assayed using ELISA techniques. The mean BMI Z-scores were -0.67, +2.15 and +3.39 for the non-obese control children, obese (BMI ≥ 90th percentile, <99th percentile) and morbidly obese (BMI ≥ 99th percentile), respectively. The plasma levels of BDNF were significantly decreased in the morbidly obese children compared with the levels in the obese and non-obese control children (507 ± 33 pg/ml vs. 626 ± 46 pg/ml, 621 ± 35 pg/ml, p < 0.05). Univariate linear regression analysis showed that the plasma level of BDNF was positively correlated with birth weight (r = 0.264, p < 0.05) and inversely correlated with the BMI Z-score (r = -0.314, p < 0.05). Multivariate forward stepwise linear regression analysis revealed that the birth weight and BMI Z-score are independent predictors of the plasma BDNF level. The plasma level of BDNF, which is decreased in morbidly obese children, is associated with birth weight and the BMI Z-score. Our results suggest that BDNF may play important roles in the development and pathophysiology of childhood obesity.

Serum levels of brain-derived neurotrophic factor (BDNF), BDNF gene Val66Met polymorphism, or plasma catecholamine metabolites, and response to mirtazapine in Japanese patients with major depressive disorder (MDD)

We investigated an association between the polymorphism of brain-derived neurotrophic factor (BDNF) gene Val66Met and the response to mirtazapine in Japanese patients with major depressive disorder (MDD). We also examined mirtazapine's effects on the serum BDNF and plasma levels of catecholamine metabolites in these patients. Eighty-four patients who met the DSM-IV-TR criteria for MDD were treated with only mirtazapine for 4 weeks. The BDNF Val66Met polymorphism was detected by direct sequencing in the region, and serum BDNF levels and plasma levels of catecholamine metabolites were measured by ELISA and HPLC-ECD, respectively. Mirtazapine treatment for 4 weeks significantly increased serum BDNF levels in the responders, whereas nonresponders showed significant decreases. No association was found between either of the two genotypes (Val/Val vs. Met-carriers) and the response to mirtazapine at T4 or the serum BDNF levels at T0. Mirtazapine did not alter the plasma levels of homovanillic acid (HVA) or 3-methoxy-4-hydroxyphenylglycol (MHPG). Discussion The dynamics of serum BDNF levels, but not plasma levels of HVA and MHPG, reflect the response to mirtazapine treatment; the BDNF Val66Met polymorphism in patients with depression is, however, associated with neither a particular response to mirtazapine treatment nor baseline serum BDNF levels. Serum BDNF levels, but not plasma levels of HVA or MHPG, and BDNF Val66Met polymorphism are related to the mirtazapine response in MDD.

Effects of voluntary running on plasma levels of neurotrophins, hippocampal cell proliferation and learning and memory in stressed rats

Previous studies have shown that a 2-week treatment with 40mg/kg corticosterone (CORT) in rats suppresses hippocampal neurogenesis and decreases hippocampal brain-derived neurotrophic factor (BDNF) levels and impairs spatial learning, all of which could be counteracted by voluntary wheel running. BDNF and insulin-like growth factor (IGF-1) have been suggested to mediate physical exercise-enhanced hippocampal neurogenesis and cognition. Here we examined whether such running-elicited benefits were accompanied by corresponding changes of peripheral BDNF and IGF-1 levels in a rat model of stress. We examined the effects of acute (5days) and chronic (4weeks) treatment with CORT and/or wheel running on (1) hippocampal cell proliferation, (2) spatial learning and memory and (3) plasma levels of BDNF and IGF-1. Acute CORT treatment improved spatial learning without altered cell proliferation compared to vehicle treatment. Acute CORT-treated non-runners showed an increased trend in plasma BDNF levels together with a significant increase in hippocampal BDNF levels. Acute running showed no effect on cognition, cell proliferation and peripheral BDNF and IGF-1 levels. Conversely, chronic CORT treatment in non-runners significantly impaired spatial learning and suppressed cell proliferation in association with a decreased trend in plasma BDNF level and a significant increase in hippocampal BDNF levels. Running counteracted cognitive deficit and restored hippocampal cell proliferation following chronic CORT treatment; but without corresponding changes in plasma BDNF and IGF-1 levels. The results suggest that the beneficial effects of acute stress on cognitive improvement may be mediated by BDNF-enhanced synaptic plasticity that is hippocampal cell proliferation-independent, whereas chronic stress may impair cognition by decreasing hippocampal cell proliferation and BDNF levels. Furthermore, the results indicate a trend in changes of plasma BDNF levels associated with a significant alteration in hippocampal levels, suggesting that treatment with running/CORT for 4 weeks may induce a change in central levels of hippocampal BDNF level, which may not lead to a significant change in peripheral levels.

Plasma Brain-Derived Neurotrophic Factor Levels Predict the Clinical Outcome of Depression Treatment in a Naturalistic Study

Remission is the primary goal of treatment for major depressive disorder (MDD). However, some patients do not respond to treatment. The main purpose of this study was to determine whether brain-derived neurotrophic factor (BDNF) levels are correlated with treatment outcomes. In a naturalistic study, we assessed whether plasma BDNF levels were correlated with clinical outcomes by measuring plasma BDNF in patients with depressive syndrome (MADRS score ≥18), and subsequently comparing levels between the subgroup of patients who underwent remission (MADRS score ≤8) and the subgroup who were refractory to treatment (non-responders). Patients with depressive syndrome who underwent remission had significantly higher plasma BDNF levels (p<0.001), regardless of age or sex. We also found a significant negative correlation between MADRS scores and plasma BDNF levels within this group (ρ = –0.287, p = 0.003). In contrast, non-responders had significantly lower plasma BDNF levels (p = 0.029). Interestingly, plasma BDNF levels in the non-responder group were significantly higher than those in the remission group in the initial stage of depressive syndrome (p = 0.002). Our results show that plasma BDNF levels are associated with clinical outcomes during the treatment of depression. We suggest that plasma BDNF could potentially serve as a prognostic biomarker for depression, predicting clinical outcome.Trial RegistrationUMIN Clinical Trials Registry UMIN000006264

Inflammation in patients with schizophrenia: the therapeutic benefits of risperidone plus add-on dextromethorphan.

Increasing evidence suggests that inflammation contributes to the etiology and progression of schizophrenia. Molecules that initiate inflammation, such as virus- and toxin-induced cytokines, are implicated in neuronal degeneration and schizophrenia-like behavior. Using therapeutic agents with anti-inflammatory or neurotrophic effects may be beneficial for treating schizophrenia. One hundred healthy controls and 95 Han Chinese patients with schizophrenia were tested in this double-blind study. Their PANSS scores, plasma interleukin (IL)-1β, tumor necrosis factor-α (TNF-α) and brain-derived neurotrophic factor (BDNF) levels were measured before and after pharmacological treatment. Pretreatment, plasma levels of IL-1β and TNF-α were significantly higher in patients with schizophrenia than in controls, but plasma BDNF levels were significantly lower. Patients were treated with the atypical antipsychotic risperidone (Risp) only or with Risp+ dextromethorphan (DM). PANSS scores and plasma IL-1β levels significantly decreased, but plasma TNF-α and BDNF levels significantly increased after 11weeks of Risp treatment. Patients in the Risp+ DM group showed a greater and earlier reduction of symptoms than did those in the Risp-only group. Moreover, Risp+ DM treatment attenuated Risp-induced plasma increases in TNF-α. Patients with schizophrenia had a high level of peripheral inflammation and a low level of peripheral BDNF. Long-term Risp treatment attenuated inflammation and potentiated the neurotrophic function but also produced a certain degree of toxicity. Risp+ DM was more beneficial and less toxic than Risp-only treatment. Protocol Record: HR-93-50; NCT01189006; URL: http://www.clinicaltrials.gov.

Robust changes in expression of brain-derived neurotrophic factor (BDNF) mRNA and protein across the brain do not translate to detectable changes in BDNF levels in CSF or plasma

Adult rats were treated acutely with peripheral kainic acid (KA), and changes in brain-derived neurotrophic factor (BDNF) mRNA and protein were tracked over time across multiple brain regions. Despite robust elevation in both mRNA and protein in multiple brain regions, plasma BDNF was unchanged and cerebrospinal fluid (CSF) BDNF levels remained undetectable. Primary neurons were then treated with KA. BDNF was similarly elevated within neurons, but was undetectable in neuronal media. Thus, while deficits in BDNF signaling have been implicated in a number of diseases, these data suggest that extracellular concentrations of BDNF may not be a facile biomarker for changes in neurons.

The concentrations of serum, plasma and platelet BDNF are all increased by treadmill VO2max performance in healthy college men

The most current human-based studies in which brain-derived neurotrophic factor (BDNF) levels in the peripheral blood system are analyzed use it as an indicator that represents BDNF levels in the CNS. However, whether circulating BDNF (serum and plasma) is positively or inversely associated with cardiorespiratory fitness levels (VO2max) is still controversial, and no study has done to investigate exercise effects on the concentration of BDNF stored in circulating platelets which, in fact, store a large amount of circulating BDNF. Thus, the purpose of this study was to determine the relation between VO2max and all circulating BDNF levels (serum, plasma and platelets) in college male students (N=18; age, 19±1 years; height, 173.22±7.65cm; weight, 78.25±14.25kg; body fat percent, 13.82±5.68%). Dual X-ray energy absorptiometry whole body scan was used to measure their body composition. After the overnight fast, all participants were performed VO2max test, and their blood was collected at rest and immediately after the exercise. Our data resulted in significant increases in platelet counts and serum, plasma and platelet BDNF levels immediately after the exercise (p<0.01). VO2max had a significant negative correlation with serum BDNF, plasma BDNF and platelet BDNF at rest (p<0.05) but a significant positive correlation with serum, plasma BDNF, and platelet BDNF immediately after the exercise (p<0.01). However, our data show no correlation between VO2max and platelet count both at rest and immediately after the exercise. In conclusion, this is the first study showing that basal BDNF levels are inversely correlated with cardiorespiratory fitness levels but that the inverse correlations turn into positive correlations with all circulating BDNF levels immediately after the exercise. Moreover, it is the first time to provide evidence that platelet BDNF levels are also positively affected by the exercise. However, future studies will be needed to investigate what tissues provide BDNF into the circulating system and to elucidate the role of circulating BDNF.

Brain-Derived Neurotrophic Factor Protects Against Cardiac Dysfunction After Myocardial Infarction via a Central Nervous System–Mediated Pathway

The central nervous system is thought to influence the regulation of the cardiovascular system in response to humoral and neural signals from peripheral tissues, but our understanding of the molecular mechanisms involved is still quite limited. Here, we demonstrate a central nervous system-mediated mechanism by which brain-derived neurotrophic factor (BDNF) has a protective effect against cardiac remodeling after myocardial infarction (MI). We generated conditional BDNF knockout mice, in which expression of BDNF was systemically reduced, by using the inducible Cre-loxP system. Two weeks after MI was induced surgically in these mice, systolic function was significantly impaired and cardiac size was markedly increased in conditional BDNF knockout mice compared with controls. Cardiomyocyte death was increased in these mice, along with decreased expression of survival molecules. Deletion of the BDNF receptor (tropomyosin-related kinase B) from the heart also led to the exacerbation of cardiac dysfunction after MI. The plasma levels of BDNF were markedly increased after MI, and this increase was associated with the upregulation of BDNF expression in the brain, but not in the heart. Ablation of afferent nerves from the heart or genetic disruption of neuronal BDNF expression inhibited the increase of plasma BDNF after MI and led to the exacerbation of cardiac dysfunction. Peripheral administration of BDNF significantly restored the cardiac phenotype of neuronal BDNF-deficient mice. These results suggest that BDNF expression is upregulated by neural signals from the heart after MI and then protects the myocardium against ischemic injury.

Association of brain-derived neurotrophic factor and tyrosine kinase B receptor in pregnancy

Abnormal brain development in a compromised prenatal and/or early postnatal environment is thought to be a risk factor for several neurobehavioural disorders. However, the mechanisms underlying these are not well understood. We have earlier reported reduced placental docosahexaenoic acid (DHA) levels in preterm deliveries. We have hypothesized that increased oxidative stress and reduced DHA levels may lead to changes in the circulating levels of maternal and cord brain-derived neurotrophic factor (BDNF) and its receptor tyrosine kinase B (TrkB) levels. A total number of 96 women delivering preterm and 95 women delivering at term were recruited. Plasma BDNF levels were measured in both mother and cord blood plasma using the BDNF Immuno Assay kit. Placental TrkB levels were analysed using sandwich enzyme-linked immunosorbent assay (ELISA). Maternal plasma BDNF levels and placental TrkB levels were higher (p<0.05) while cord plasma BDNF levels were lower (p<0.01) in women delivering preterm as compared to term. There was a negative association between levels of placental TrkB and DHA (p=0.034). A negative association between maternal plasma BDNF levels and placental weight (p=0.001) was observed while a positive association was seen between cord plasma BDNF levels and gestation (p=0.025). The reduction in cord BDNF levels may have implications for altered neurodevelopment in childhood and later life. Studies need to be undertaken to follow up children born preterm for risk of neurobehavioural disorders like attention deficit hyperactivity disorder (ADHD) to understand the effect of altered BDNF at birth on neurodevelopment.

Plasma BDNF Is Associated with Age-Related White Matter Atrophy but Not with Cognitive Function in Older, Non-Demented Adults

Brain derived neurotrophic factor (BDNF) seems to be involved in regulation of synaptic plasticity and neurogenesis. BDNF plasma and serum levels have been associated with depression, Alzheimer's disease, and other psychiatric and neurodegenerative disorders. In a community sample, drawn from the Baltimore Longitudinal Study of Aging (BLSA), we examined whether BDNF plasma concentration was associated with rates of age-related change in cognitive performance (n = 429) and regional brain volume (n = 59). Plasma BDNF levels, which were significantly higher in females (p<0.05), were not associated with either concurrent cognitive performance or rates of age-related change in performance across cognitive domains (p's>0.05). Sex differences in the relationship between BDNF and the trajectories of regional brain volume changes were observed for the whole brain and frontal white matter volumes (p<0.05), whereby lower plasma BDNF was associated with steeper volume decline in females but not males. Together, our findings contribute to furthering the understanding of the relationships between plasma BDNF, structural brain integrity and cognition. Potential mechanisms mediating these relationships merit further investigation.

Brain‐Derived Neurotrophic Factor Intensifies the Early Inflammatory Response After Myocardial Infarction

Plasma brain‐derived neurotrophic factor (BDNF) levels correlate positively with indices of metabolic and cardiovascular disease, but role of BDNF in the cardiac response to myocardial infarction (MI) has not been investigated. BDNF heterozygous (HET) mice become obese and insulin resistant with age. We hypothesized that 50% reduced levels of BDNF would impair post‐MI cardiac remodeling. We compared 7–9 month old male C57BL/6J wild type (WT) and HET mice (n=11/group) at day 0 and days 1,3,5 and 7 post‐MI (n=11–18/group). WT and HET mice had similar infarct sizes (43–50±2% for 1–7 days MI). Plasma proteomic profiling at day 1 post‐MI revealed that, monocyte chemotactic protein (MCP)‐1 (177±pg/ml in WT and 228±25pg/ml in HET) and MCP‐5 (38±4pg/ml in WT and 49±5pg/ml in HET) levels were enhanced in the HET mice, compared to day 0 controls and WT day 1 levels (p&lt;0.05). By inflammatory RT2‐PCR array, the mRNA expression of MCP‐1 and MCP‐5 were also increased in HET compared to WT at day 1 (p&lt;0.05). Interestingly, matrix metalloproteinase‐9 (129±11ng/ml in WT and 96±4ng/ml in HET) and myeloperoxidase (183±13ng/ml in WT and 147±7ng/ml in HET) levels increase in WT plasma post‐MI, and these increases were attenuated in HET mice at day 1 (p&lt;0.05). Our finding demonstrates that reduced BDNF in the post‐MI setting modifies the early inflammatory response to MI, potentially by altering neutrophil and macrophage kinetics. Funding support ‐ NIH/NHLBI/NCCAM and the VA.

Recovery of low plasma BDNF over the course of treatment among patients with bulimia nervosa

Recent studies have suggested that brain-derived neurotrophic factor (BDNF) is associated with energy balance, eating behaviors, and psychological states such as depression. Although decreased BDNF levels in patients with bulimia nervosa (BN) have been reported, the mechanism is still unclear. Few studies have investigated longitudinal changes of BDNF in BN patients. We investigated changes in the levels of plasma BDNF before and after inpatient treatment. Subjects were 16 female patients with BN and 10 control females. The levels of plasma BDNF were measured. In seven patients who completed a 4-week inpatient treatment program based on cognitive behavior therapy, levels of plasma BDNF were measured twice, before and after inpatient treatment. Plasma BDNF levels were significantly lower in BN subjects than in controls. BDNF levels were significantly higher following inpatient treatment. Increased plasma BDNF after inpatient treatment suggests that lower plasma BDNF levels in BN patients are associated with abnormal eating behaviors, especially binge eating.

Polycystic ovary syndrome: brain-derived neurotrophic factor (BDNF) plasma and follicular fluid levels

Polycystic ovary syndrome is one of the most common endocrine disorders in women of reproductive age. Features of PCOS are hyperandrogenism, chronic anovulation and polycystic ovaries on ultrasonography. Follicle development is a complex and carefully orchestrated phenomenon, involving gonadotropins and a rapidly expanding list of other intraovarian regulators, such as brain-derived neurotrophic factor (BDNF). The aim of this study is to evaluate BDNF in plasma and in follicular fluid in women affected by PCOS and in normal menstruating women. In PCOS patients the BDNF levels in plasma and in follicular fluid are higher than values obtained in healthy controls. Therefore we can hypothsize that high levels of luteinizing hormone, probably increase the secretion of BDNF in PCOS patients.