Brain-derived Neurotrophic Factor In Groups Research Articles

BDNF, proBDNF and proBDNF/BDNF ratio with electroencephalographic abnormalities in children with attention deficit hyperactivity disorder: Possible relations to cognition and severity.

Attention deficit hyperactivity disorder (ADHD) with and without subclinical epileptogenic discharges (SED) have been suggested to negatively affect cognitive abilities of children with ADHD. The role of brain-derived neurotrophic factor (BDNF) and its precursor proBDNF in ADHD is in need of being investigated. The aims were to evaluate the levels of serum BDNF, proBDNF and the proBDNF/BDNF ratio in addition to the potential impacts of SED on the children's cognitive abilities and the severity of ADHD. The included participants with ADHD were 30 children with normal electroencephalogram (EEG) (G1) and 30 children with SED (G2), together with 30 healthy children (G3). The cognitive abilities and severity of the disorder were evaluated. The biochemical measures were determined by ELISA. The presence of coexisting SED and nocturnal enuresis has led to a deleterious effect on cognitive processes but not on the severity. The focal epileptogenic discharge was the most common among children in G2. The levels of BDNF in Groups 1 and 2 were less than those in G3. The higher proBDNF/BDNF ratio could be related to the low BDNF levels rather than high proBDNF levels. The findings of this study highlight the importance of investigating the presence of SED and nocturnal enuresis in children with ADHD. Targeting strengthening of cognitive abilities in children with coexisting ADHD and SED is advised. The role of proBDNF in the pathophysiology of ADHD needs further investigation.

The mechanism of mesenchymal stem cells on neural function in rats with traumatic brain injury

Objective To investigate the effect of mesenchymal stem cells (MSCs) on the neurological function of rats with traumatic brain injury, and to investigate the mechanism of the effect of MSCs. Methods 60 SD rats models with brain injury established by the modified Feeney method were divided into model group, MSCs group and phosphate buffer (PBS) group by. Another 20 healthy SD rats were chosen as the control group. Rats of MSCs group were transplantated with Umbilical cord mesenchymal stem cells isolated and cultured in vitro. Neurological function of rats in each group were evaluated by improved neurological function score (mNSS) standard at 1, 3, 7, 14, 21, 28 d after transplantation. Neuronal nuclear antigen (NeuN) expression level in the brain tissue of rats was detected with immunohistochemical method. Brain-derived neurotrophic factor (BDNF) mRNA level of in the brain tissue of rats was detected with reverse transcriptase-polymerase chain reaction (RT-PCR) method. The apoptosis level of cerebral tissue cells in rats was detected by TdT-mediated dUTP nick end labeling (TUNEL) method. Results Compared with the control group, mNSS score of rats in model group, MSCs group and PBS group increased, NeuN expression decreased increased (P=0.000). Compared with the model group and PBS group, mNSS score of rats in MSCs group significantly decreased, NeuN expression significantly decreased(P=0.000). Compared with the control group BDNF mRNA level (0.31±0.12), BDNF mRNA level in model group, PBS group and MSCs Group (1.32±0.34, 1.23±0.30, 0.81±0.21) significantly increased (P=0.000). Compared with model group and PBS group, the levels of BDNF mRNA in MSCs group significantly reduced (P=0.014, P=0.019). Compared with the apoptosis level of brain tissue in control group (3.14±1.12), apoptosis level in model group, PBS group and MSCs group (27.84±4.32, 25.35±4.89, 10.33±3.32) significantly increased (P=0.000). Compared with model group and PBS group, the level of apoptosis in brain tissue of MSCs group significantly decreased (P=0.000). Conclusion Mesenchymal stem cells can decreased the apoptosis level of brain injury in rats through the mechanism of repairing damaged neurons and promoting the BDNF secretion. It can promote the repair effect on neural function of rats with traumatic brain injury. Key words: Brain injury; Mesenchymal stem cells; Nerve function

Physical therapy intervention (PTI) increases plasma brain-derived neurotrophic factor (BDNF) levels in non-frail and pre-frail elderly women

Biomarkers are important factors in the identification of the frail elderly (higher risk of developing disease) and in assessing the impact of PTI. On the other hand, BDNF has been related to neuroprotection in a series of central nervous system diseases in older age. The levels of BDNF in groups of elderly women classified according to Fried phenotype (non-frail and pre-frail) were compared. We assessed the impact of a PTI on BDNF levels. A convenience sample of 48 elderly women was randomly selected. The PTI group was composed by 20 elderly women selected from this group. Plasma neurotrophic factors, such as BDNF, glial-derived neutrophic factor (GDNF), and nerve growth factor (NGF) were measured by enzyme-linked immunosorbent assay (ELISA). Timed-up-and-go (TUG) test, hand-grip and work/body weight were evaluated before and after the intervention. Plasma concentrations of BDNF were significantly higher in non-frail in comparison to pre-frail elderly women. After the PTI, higher levels of BDNF were found in elderly women (before 351±68pg/ml and after 593±79pg/ml; p<0.001). Both groups had an increase in BDNF levels after the PTI. The low levels of BDNF in pre-frail elderly women suggest that this neurotrophic factor may be a key pathophysiological mediator in the syndrome of frailty. The fact that PTI increased BDNF levels in both groups suggests that it may be possible to modify this phenotype.

Brain-derived neurotrophic factor promotes bovine oocyte cytoplasmic competence for embryo development

The ability of an oocyte to support early embryonic development requires both nuclear and cytoplasmic maturation. We have investigated the effects of brain-derived neurotrophic factor (BDNF) on maturation of the bovine oocyte and embryo development after parthenogenetic activation. By RT-PCR and immunohistochemistry, cumulus and oocytes were shown to express mRNA and protein for BDNF and the p75 common neurotrophin receptor. However, mRNA for the BDNF-specific full length and truncated isoforms of the TrkB receptor are only detected in cumulus, suggesting that oocytes and cumulus differ in their capacity to respond to neurotrophin signalling. In in vitro maturation experiments, the proportion of cumulus oocyte complexes maturing to metaphase II was not altered by BDNF in groups lacking fetal calf serum (FCS), but was significantly lower than the positive control containing 10% FCS (P < 0.01). However, after maturation, the proportion of parthenogenetically activated oocytes forming blastocysts was highest for 10 ng/ml BDNF (24%, n = 95) followed by 100 ng/ml BDNF (18%, n = 91) and 10% FCS (15%, n = 103), which in turn were greater than no serum (10%, n = 83; P < 0.01). Maturation in the presence of a BDNF blocking antibody resulted in a blastocyst yield that was comparable to the absence of serum, and lower than in the presence of BDNF (P < 0.01). Similar effects on progression to metaphase II and blastocyst formation were observed using oocytes matured without cumulus. Together, these results provide the first evidence for a role for neurotrophins in promoting oocyte cytoplasmic competence to support embryonic development, despite being insufficient in the absence of serum to enhance nuclear maturation.