Expression Patterns of miRNAs in Egyptian Children with ADHD: Clinical Study with Correlation Analysis

Changes in plasma müllerian-inhibiting substance and brain-derived neurotrophic factor after chemotherapy in premenopausal women

Plasma brain-derived neurotrophic factor in women after bariatric surgery: a pilot study

Lower plasma DHEAS and BDNF levels as indicators of cognitive decline.

In adult rat brains, brain-derived neurotrophic factor (BDNF) rhythmically oscillates according to the light-dark cycle and exhibits unique functions in particular brain regions. However, little is known of this subject in juvenile rats. Here, we examined diurnal variation in BDNF and neurotrophin-3 (NT-3) levels in 14-day-old rats. BDNF levels were high in the dark phase and low in the light phase in a majority of brain regions. In contrast, NT-3 levels demonstrated an inverse phase relationship that was limited to the cerebral neocortex, including the visual cortex, and was most prominent on postnatal day 14. An 8-h phase advance of the light-dark cycle and sleep deprivation induced an increase in BDNF levels and a decrease in NT-3 levels in the neocortex, and the former treatment reduced synaptophysin expression and the numbers of synaptophysin-positive presynaptic terminals in cortical layer IV and caused abnormal BDNF and NT-3 rhythms 1 week after treatment. A similar reduction of synaptophysin expression was observed in the cortices of Bdnf gene-deficient mice and Ca(2+)-dependent activator protein for secretion 2 gene-deficient mice with abnormal free-running rhythm and autistic-like phenotypes. In the latter mice, no diurnal variation in BDNF levels was observed. These results indicate that regular rhythms of BDNF and NT-3 are essential for correct cortical network formation in juvenile rodents.

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

BDNF expression mediates verbal learning and memory in women in a cohort enriched with risk for Alzheimer's disease.

Objective Glioblastomas (GBMs) are among the most frequent and most malignant of untreatable brain tumors. A GBM marker could accelerate diagnosis and facilitate therapeutic monitoring. This prospective, observational, controlled study compared brain-derived neurotrophic factor (BDNF) levels in cerebrospinal fluid (CSF) and plasma between patients with GBM and a control group. Materials and methods Patients in the observational group underwent elective GBM resection (n=24, 55.8%).Control patients (n=19, 44.2%) had elective brain surgery for an unrelated, non-neoplastic, non-traumatic pathology. We measured BDNF levels in tumors, CSF, and plasma with enzyme-linked immunosorbent assay (ELISA). Peripheral blood and CSF samples were collected before surgery, and tumors were sampled intraoperatively. We analyzed correlations between BDNF levels and patient sex, age, seizures, smoking, diabetes mellitus (DM), and the use of selected antiepileptic drug (AED) and antihypertensive drug groups. Results The mean CSF BDNF concentration was significantly lower in patients with GBM (6.5 pg/mL) than in controls (11.48 pg/mL) (p=0.002). Similarly, the mean plasma BDNF concentration was significantly lower in patients with GBM (288.59 pg/mL) than in controls (574.06 pg/mL) (p=0.0005). None of the examined factors influenced CSF, plasma, or tumor tissue BDNF concentrations (p>0.05). Conclusion Plasma and CSF BDNF levels were significantly lowerin adults with GBM than in controls. Thus, CSF and plasma BDNF levels may aid in GBM diagnoses. Further prospective studies are required.

The involvement of brain-derived neurotrophic factor (BDNF) in rheumatoid arthritis (RA) is largely unknown. The distribution of BDNF and its associated receptors, TrkB and p75, in the synovial tissue of patients with RA was examined and contrasted with that in patients with osteoarthritis (OA). Additionally, levels of BDNF in both synovial tissue and synovial fluid were measured. Furthermore, the effects of anti-tumour necrosis factor (anti-TNF; infliximab) treatment on BDNF levels in the plasma of RA patients were analysed. Cells in the synovium showed immunoreactivity for BDNF and BDNF-, p75- and TrkB-receptor immunoreactions were seen in nerve fibres of nerve fascicles and in association with sensory corpuscles. The levels of BDNF in synovial tissue were not correlated with the number of inflammatory cells observed microscopically or with levels of TNFalpha. Nor did the BDNF levels in synovial fluid correlate with erythrocyte sedimentation rate (ESR) or white blood cell counts. Anti-TNF treatment lead to a decrease in plasma levels of BDNF 14 weeks after the initiation of anti-TNF therapy, i.e., 8 weeks after the last infusion. Higher levels of BDNF were observed in RA patients at baseline compared with those for healthy individuals. However, the levels of BDNF in plasma of patients treated with anti-TNF did not correlate with the changes in ESR or a disease activity score. The clinical significance of this study is that anti-TNF treatment influences plasma levels of BDNF although there was no evidence that BDNF levels correlate with inflammatory parameters in either infliximab-treated or non-infliximab-treated patients with RA. Instead it is likely that sources other than inflammatory cells, including nerve structures, are important sources of BDNF and that the effects of anti-TNF treatment on BDNF levels may be related to effects on circulating and various local cells and/or BDNF-containing neurons.

Plasma brain-derived neurotrophic factor (BDNF) levels are associated with the hormonal status of women. Moreover, the suprachiasmatic nucleus appears to be implicated in the modulation of BDNF central levels. We aimed to investigate whether BDNF circadian rhythms exist in women and if there is a relationship with cortisol circadian rhythmicity. Moreover, we aimed to establish whether the hormonal status influences BDNF diurnal variations. A total of 30 women were studied: 10 fertile ovulatory women, 10 women undergoing oral contraceptive (OC) therapy and 10 post-menopausal women. Basal BDNF and estradiol levels were assayed in blood samples collected after overnight fasting at regular intervals (08:00, 12:00, 16:00, 20:00, 24:00). BDNF and cortisol levels were measured in samples collected during the follicular and luteal phases in ovulatory women and once a month in OC and post-menopausal women. Luteal BDNF levels were significantly higher than follicular levels in fertile women (P < 0.001). In OC women, BDNF levels were similar to the follicular BDNF levels, whereas in post-menopausal women, they were significantly lower (P < 0.001). BDNF showed a diurnal rhythm in the follicular phase and in women undergoing OC, although the diurnal rhythm was blunted in the luteal phase. In post-menopausal women, BDNF and cortisol levels significantly decreased during the day. BDNF has a diurnal variation in women that is somewhat analogous to cortisol variation; however, the amplitude of the variation in BDNF levels appears to be influenced by ovarian function. Interactions between BDNF, the hypothalamus-pituitary-adrenal axis and sex steroids might play a critical role in the human homeostasis and adaptation.

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

included 35 studies with a total of 2238 patients with BD, and 1560 healthy controls. Levels of BDNF were lower in crude blood samples from BD patients (P = 0.02), as well as in the serum of manic (P = 0.01) and depressed patients (P = 0.002), compared with healthy control subjects. No differences in peripheral BDNF levels were observed in any of the affective states. Furthermore, a longer illness duration was associated with higher BDNF levels in BD patients [6]. The BDNF enzyme-linked immunosorbent assay (ELISA) kits used in early reports recognized both proBDNF and mature BDNF, due to the limited specificity of the BDNF antibody [7]. Using new, commercial human BDNF ELISA kits capable of differentiating between proBDNF and mature BDNF, we reported high concentrations of both BDNF forms in human serum [7, 8] (Table 1). Serum levels of proBDNF in approximately 38 percent of the healthy Japanese control subjects were less than the minimum detectable concentration (0.5 ng/mL) of the kit (Table 1) [8]. Noting the high concentrations and putative opposing functions of proBDNF and mature BDNF, authors have focused their attention on the separate measurements of these factors in human blood [2, 9, 10]. Sodersten et al. [11] reported that serum levels of mature BDNF in mood-stabilized patients with BD were significantly higher than in healthy controls, whereas serum levels of proBDNF in BD patients were significantly lower than those of controls (Swedish samples) [11]. In this study, serum levels of proBDNF could be measured in all healthy control subjects (Table 1) [11]. In contrast, serum levels of mature BDNF in depressed patients were significantly lower than those of healthy controls [8]. It is therefore possible that measuring blood levels of mature BDNF and proBDNF could provide a method for distinguishing between depression and BD, thus reducing the high rates of misdiagnosis between these diseases Brain-derived neurotrophic factor (BDNF), a major neurotrophic factor in the brain, plays an important role in the pathophysiology of mood disorders, such as depression and bipolar disorder (BD) [1–3]. BDNF (mature BDNF) is a 13-kDa polypeptide, synthesized initially as a precursor protein, preproBDNF, in the endoplasmic reticulum. Following cleavage of its signal peptide, proBDNF (~32 kDa) is converted to mature BDNF by intracellular or extracellular proteases. It was first thought that only secreted, mature BDNF possessed biological activity, and that proBDNF, which localizes intracellularly, served as an inactive precursor. However, accumulating evidence demonstrates that both proBDNF and mature BDNF are active, eliciting opposing effects via the p75 and TrkB receptors, respectively, and that both forms play a key role in several physiological functions [2, 3]. In 2003, we reported that serum levels of BDNF in drugnaive patients with depression were significantly lower than those of healthy controls [4]. Since then, a number of studies have replicated our initial finding. A recent meta-analysis of 179 associations (N = 9484 subjects) showed that serum levels of total BDNF (mature BDNF and proBDNF), in antidepressant-free patients with depression were significantly lower (Cohen’s d = −0.71, P < 0.0000001) than those of healthy controls [5]. Furthermore, Munkholm et al. [6] performed a systematic and quantitative metaanalysis of BDNF (mature BDNF and proBDNF) levels in blood samples from patients with BD. This analysis

Low Brain-Derived Neurotrophic Factor (BDNF) levels in serum of depressed patients probably results from lowered platelet BDNF release unrelated to platelet reactivity

Elevated plasma brain-derived neurotrophic factor as a potential risk biomarker for major depressive disorder in middle-aged women: A nested case-control study.

BackgroundWhereas brain-derived neurotrophic factor (BDNF) levels are measured in the brain in animal models of stroke, neurotrophin levels in stroke patients are measured in plasma or serum samples. The present study was designed to investigate the meaning of circulating BDNF levels in stroke patients.Methods and ResultsUnilateral ischemic stroke was induced in rats by the injection of various numbers of microspheres into the carotid circulation in order to mimic the different degrees of stroke severity observed in stroke patients. Blood was serially collected from the jugular vein before and after (4 h, 24 h and 8 d) embolization and the whole brains were collected at 4, 24 h and 8 d post-embolization. Rats were then selected from their degree of embolization, so that the distribution of stroke severity in the rats at the different time points was large but similar. Using ELISA tests, BDNF levels were measured in plasma, serum and brain of selected rats. Whereas plasma and serum BDNF levels were not changed by stroke, stroke induced an increase in brain BDNF levels at 4 h and 24 h post-embolization, which was not correlated with stroke severity. Individual plasma BDNF levels did not correlate with brain levels at any time point after stroke but a positive correlation (r = 0.67) was observed between individual plasma BDNF levels and stroke severity at 4 h post-embolization.ConclusionCirculating BDNF levels do not mirror brain BDNF levels after stroke, and severe stroke is associated with high plasma BDNF in the very acute stage.

BackgroundNormal cognitive status is essential for daily activities, but many people with chronic autoimmune rheumatic diseases are impaired in this function. This is probably related to the age of the...