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Sedentary patterns are associated with BDNF in patients with type 2 diabetes mellitus.
Júdice, PB, Magalhães, JP, Hetherington-Rauth, M, Correia, IR, Sardinha, LB
European journal of applied physiology. 2021;(3):871-879
Abstract
PURPOSE Exercise is beneficial to type-2 diabetes-mellitus (T2DM), and there is evidence showing that one of those benefits include a higher expression of brain-derived neurotrophic factor (BDNF), which has been implicated in improving fat oxidation and cognitive development. The deleterious effect of prolonged sedentary time (ST) on BDNF levels has never been examined in patients with T2DM. Our goal was to analyse the associations for sedentary patterns [i.e. breaks in ST per sedentary hour (BST-ST) and bouts of sedentary time (BSB) of different length] with BDNF in patients with T2DM, independent of moderate-to-vigorous physical activity (MVPA) and cardiorespiratory fitness (CRF). METHODS Sample included 80 patients (38 women) with T2DM (58.3 ± 7.8 years). ST and MVPA were assessed by accelerometry (ActiGraph, GT3X + model), BDNF by blood collection and plasma quantification using commercial enzyme-linked immunosorbent assay kits, and CRF was determined using a Bruce protocol to exhaustion, on a motorized treadmill. RESULTS Positive associations for BST-ST (β = 0.155; p = 0.007) with BDNF, and negative associations for BSB longer than 15 min with BDNF were found (β = - 0.118; p = 0.049). Neither MVPA nor cardiorespiratory fitness eliminated the associations for BST-ST with BDNF, but MVPA eradicated the associations between BSB > 15 min and BDNF. CONCLUSIONS Our findings suggest that interrupting ST and especially avoiding longer sedentary periods (> 15 min) may be beneficial for BDNF plasma abundance that may influence metabolic and cognitive functioning of patients with T2DM, especially for the ones presenting lower MVPA levels. TRIAL REGISTRATION May 5, 2017, ClinicalTrials.govID:NCT03144505.
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2.
Interaction between dietary total antioxidant capacity and BDNF Val66Met polymorphism on lipid profiles and atherogenic indices among diabetic patients.
Abaj, F, Rafiee, M, Koohdani, F
Scientific reports. 2021;(1):19108
Abstract
Brain-derived neurotrophic factor (BDNF) belongs to the "neurotrophin" family of growth factors, and it has recently been associated to cardiovascular disease (CVD). We anticipated that BDNF Val66Met polymorphisms may alter CVD risk markers such as serum lipid profile differences, and interaction with total antioxidant capacity of diet (DTAC) could alter these clinical parameters. This cross-sectional study consisted of 667 diabetic patients (39.7% male and 60.3% female). DTAC was calculated by international databases. Biochemical markers including total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglyceride (TG), superoxide dismutase (SOD), C-reactive protein (CRP), total antioxidant capacity (TAC), pentraxin-3 (PTX3), isoprostaneF2α (PGF2α). interleukin 18 (IL18), leptin and ghrelin were measured by standard protocol. Atherogenic indices (AIP, AC, CR-I, CR-II) were calculated. Genotyping of the BDNF Val66Met polymorphisms was conducted by the real-time PCR-RFLP method. The gene-diet interactions were evaluated using a generalized linear mode (GLMs). Carriers of the Val/Met genotype who were in the higher median intake of FRAP had lower HDL (P:0.04) and higher TG (P:0.005), AIP (P:0.02) and AC (P:0.02) index compared to Val/Val genotypes with lower median intake. Moreover, diabetic patients with Val/Met genotype who consumed higher ORAC intake had increased odds for anthropometric indices (BMI (P:0.01) and WC (P:0.03)), lipid profiles (TG) (P:0.01), and atherogenic index (AIP) (P:0.02), also decreased odds for HDL (P:0.03) concentration compared to reference group whit lower ORAC intake. Individuals with Val/Met genotype who consumed higher TRAP intake had increased odds for WC (P:0.04), TC (P:0.001), TG (P < 0.001), AIP (P < 0.001) and AC (P < 0.001). Finally, Val/Met patients with a higher median intake of TEAC had higher TG (P:0.02), AIP (P:0.009) and AC (P:0.03) compared to the reference group whit lower TEAC intake. Our study showed that Val/Met genotype had also the highest lipid profile and atherogenic indices even in the highest adherence to DTAC. While it seems that the presence of the Val/Val wild-type and BDNF Met/Met homozygotes in diabetic patients with a high DTAC is a protective factor.
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Screen time is independently associated with serum brain-derived neurotrophic factor (BDNF) in youth with obesity.
Goldfield, GS, Cameron, JD, Sigal, RJ, Kenny, GP, Holcik, M, Prud'homme, D, Guerin, E, Alberga, AS, D'Angiulli, A, Tremblay, MS, et al
Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme. 2021;(9):1083-1090
Abstract
Low levels of brain derived-neurotrophic factor (BDNF) and excessive screen exposure are risk factors for neurocognitive deficits and obesity in youth, but the relationship between screen time and BDNF remains unknown. This study examined whether duration and/or type of sedentary screen time behaviour (TV viewing, video games, recreational computer use) are associated with serum BDNF levels in youth with obesity. The sample consisted of 250 inactive, postpubertal adolescents with obesity (172 females/78 males, aged 15.5 ± 1.4 years) at the baseline assessment of the Healthy Eating, Aerobic, Resistance Training in Youth Study. After controlling for self-reported age, sex, race, parental education, puberty stage, physical activity, and diet, higher total screen exposure was significantly associated with lower serum BDNF levels (β = -0.21, p = 0.002). TV viewing was the only type of screen behaviour that was associated with BDNF levels (β = -0.22, p = 0.001). Higher exposure to traditional forms of screen time was independently associated with lower serum BDNF levels, and this association appears to be driven primarily by TV viewing. Future intervention research is needed to determine whether limiting screen time is an effective way to increase BDNF and associated health benefits in a high-risk population of youth with obesity. Trial Registration: ClinicalTrials.Gov NCT00195858. Novelty: This study is the first to show that recreational screen time is inversely associated with serum BDNF levels. The inverse association between screen time and BDNF is driven primarily by TV viewing, indicating the type of screen might matter.
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Perisynaptic astrocytes as a potential target for novel antidepressant drugs.
Frizzo, ME, Ohno, Y
Journal of pharmacological sciences. 2021;(1):60-68
Abstract
Emerging evidence suggests that dysfunctions in glutamatergic signaling are associated with the pathophysiology of depression. Several molecules that act on glutamate binding sites, so-called glutamatergic modulators, are rapid-acting antidepressants that stimulate synaptogenesis. Their antidepressant response involves the elevation of both extracellular glutamate and brain-derived neurotrophic factor (BDNF) levels, as well as the postsynaptic activation of the mammalian target of rapamycin complex 1. The mechanisms involved in the antidepressant outcomes of glutamatergic modulators, including ketamine, suggest that astrocytes must be considered a cellular target for developing rapid-acting antidepressants. It is well known that extracellular glutamate levels and glutamate intrasynaptic time-coursing are maintained by perisynaptic astrocytes, where inwardly rectifying potassium channels 4.1 (Kir4.1 channels) regulate both potassium and glutamate uptake. In addition, ketamine reduces membrane expression of Kir4.1 channels, which raises extracellular potassium and glutamate levels, increasing postsynaptic neural activities. Furthermore, inhibition of Kir4.1 channels stimulates BDNF expression in astrocytes, which may enhance synaptic connectivity. In this review, we discuss glutamatergic modulators' actions in regulating extracellular glutamate and BDNF levels, and reinforce the importance of perisynaptic astrocytes for the development of novel antidepressant drugs.
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The Influence of Val66Met Polymorphism in Brain-Derived Neurotrophic Factor on Stroke Recovery Outcome: A Systematic Review and Meta-analysis.
Liu, X, Fang, JC, Zhi, XY, Yan, QY, Zhu, H, Xie, J
Neurorehabilitation and neural repair. 2021;(6):550-560
Abstract
Background and purpose. A single nucleotide polymorphism at nucleotide 196 (G/A) in the human brain-derived neurotrophic factor (BDNF) gene produces an amino acid substitution (valine to methionine) at codon 66(Val66Met). It is unclear whether carriers of this substitution may have worse functional outcomes after stroke. We aimed to explore the distribution of Val66Met polymorphism and evaluate the effect of different genotypes on stroke functional recovery. Methods. Several databases were searched using the keywords BDNF or brain-derived neurotrophic factor, codon66, G196A, rs6265, or Val66Met, and stroke. Results. A total of 25 articles were relevant to estimate the distribution of alleles; 5 reports were applied in the meta-analysis to assess genetic differences on recovery outcomes. The genetic model analysis showed that the recessive model should be used; we combined data for AA versus GA+GG (GG-Val/Val, GA-Val/Met, AA-Met/Met). The results showed that stroke patients with AA might have worse recovery outcomes than those with GA+GG (odds ratio = 1.90; 95% CI: 1.17-3.10; P = .010; I2 = 69.2%). Overall, the A allele may be more common in Asian patients (48.6%; 95% CI: 45.8%-51.4%, I2 = 54.2%) than Caucasian patients (29.8%; 95% CI: 7.5%-52.1%; I2 = 99.1%). However, in Caucasian patients, the frequency of the A allele in Iranians (87.9%; 95% CI: 83.4%-92.3%) was quite higher than that in other Caucasians (18.7%; 95% CI: 16.6%-20.9%; I2 = 0.00%). Conclusion. Val66Met AA carriers may have worse rehabilitation outcomes than GA+GG carriers. Further studies are needed to determine the effect of Val66Met polymorphism on stroke recovery and to evaluate this relationship with ethnicity, sex, age, stroke type, observe duration, stroke severity, injury location, and therapies.
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A reconciling hypothesis centred on brain-derived neurotrophic factor to explain neuropsychiatric manifestations in rheumatoid arthritis.
Pedard, M, Quirié, A, Tessier, A, Garnier, P, Totoson, P, Demougeot, C, Marie, C
Rheumatology (Oxford, England). 2021;(4):1608-1619
Abstract
Rheumatoid arthritis (RA) is an autoimmune chronic inflammatory disease characterized by synovitis leading to joint destruction, pain and disability. Despite efficient antirheumatic drugs, neuropsychiatric troubles including depression and cognitive dysfunction are common in RA but the underlying mechanisms are unclear. However, converging evidence strongly suggests that deficit in brain-derived neurotrophic factor (BDNF) signalling contributes to impaired cognition and depression. Therefore, this review summarizes the current knowledge on BDNF in RA, proposes possible mechanisms linking RA and brain BDNF deficiency including neuroinflammation, cerebral endothelial dysfunction and sedentary behaviour, and discusses neuromuscular electrical stimulation as an attractive therapeutic option.
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The role of physical exercise in modulating peripheral inflammatory and neurotrophic biomarkers in older adults: A systematic review and meta-analysis.
Titus, J, Bray, NW, Kamkar, N, Camicioli, R, Nagamatsu, LS, Speechley, M, Montero-Odasso, M
Mechanisms of ageing and development. 2021;:111431
Abstract
BACKGROUND Physiological cascades of neurotrophic factors and inflammatory cytokines may mediate the exercise-induced amelioration of cognition in older adults. However, there is limited understanding on how different exercise modalities improving cognition alter biomarkers. Our aim was to evaluate the effects of different exercise modalities on blood biomarker concentrations in cognitive clinical trials of older adults. METHODS A systematic review (SR) and meta-analysis (MA) were performed using the databases PubMed, EMBASE, and SCOPUS. After exclusions, 17 trials with 18 distinct exercise interventions were included. RESULTS Aerobic training increased (n = 2) or did not significantly change BDNF (n = 5), and resistance training increased (n = 2) or did not significantly change (n = 2) IGF-1. Multimodal training significantly increased (n = 1) or did not change (n = 3) BDNF. Interventions that recruited sex-specific cohorts showed an advantage in males for blood marker concentrations and cognitive performance outcomes (n = 3) compared to females (n = 3). Only one of three interventions decreased concentrations of CRP. Eight studies examining BDNF changes were suited for MA and showed that higher BDNF concentrations were reached post intervention, although not reaching statistical significance (p = .26, I2 = 44 %). DISCUSSION Our results suggest that exercise has potential to ameliorate cognitive decline in older adults with divergent, modality-specific, neurotrophic mechanisms.
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Plasma brain-derived neurotrophic factor and dynamic cerebral autoregulation in acute response to glycemic control following breakfast in young men.
Tsukamoto, H, Ishibashi, A, Marley, CJ, Shinohara, Y, Ando, S, Bailey, DM, Hashimoto, T, Ogoh, S
American journal of physiology. Regulatory, integrative and comparative physiology. 2021;(1):R69-R79
Abstract
We examined the acute impact of both low- and high-glycemic index (GI) breakfasts on plasma brain-derived neurotrophic factor (BDNF) and dynamic cerebral autoregulation (dCA) compared with breakfast omission. Ten healthy men (age 24 ± 1 yr) performed three trials in a randomized crossover order; omission and Low-GI (GI = 40) and High-GI (GI = 71) breakfast conditions. Middle cerebral artery velocity (transcranial Doppler ultrasonography) and arterial pressure (finger photoplethysmography) were continuously measured for 5 min before and 120 min following breakfast consumption to determine dCA using transfer function analysis. After these measurements of dCA, venous blood samples for the assessment of plasma BDNF were obtained. Moreover, blood glucose was measured before breakfast and every 30 min thereafter. The area under the curve of 2 h postprandial blood glucose in the High-GI trial was higher than the Low-GI trial (P < 0.01). The GI of the breakfast did not affect BDNF. In addition, both very-low (VLF) and low-frequency (LF) transfer function phase or gains were not changed during the omission trial. In contrast, LF gain (High-GI P < 0.05) and normalized gain (Low-GI P < 0.05) were decreased by both GI trials, while a decrease in VLF phase was observed in only the High-GI trial (P < 0.05). These findings indicate that breakfast consumption augmented dCA in the LF range but High-GI breakfast attenuated cerebral blood flow regulation against slow change (i.e., the VLF range) in arterial pressure. Thus we propose that breakfast and glycemic control may be an important strategy to optimize cerebrovascular health.
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Effect of synbiotic and probiotic supplementation on serum brain-derived neurotrophic factor level, depression and anxiety symptoms in hemodialysis patients: a randomized, double-blinded, clinical trial.
Haghighat, N, Rajabi, S, Mohammadshahi, M
Nutritional neuroscience. 2021;(6):490-499
Abstract
BACKGROUND The aim of this study was to investigate the effects of probiotic and synbiotic supplementation on the depression and anxiety symptoms and serum brain-derived neurotrophic factor (BDNF) level. METHODS Seventy-five HD patients were randomly assigned to receive the synbiotic (15 g of prebiotics, 5 g of probiotic containing Lactobacillus acidophilus T16, Bifidobacterium bifidum BIA-6, Bifidobacterium lactis BIA-7, and Bifidobacterium longum BIA-8 (2.7 × 107 CFU/g each)) or probiotics (5 g probiotics as in synbiotic group with 15 g of maltodextrin as placebo) or placebo (20 g of maltodextrin) for 12 weeks. Serum BDNF was measured by ELISA kit. Hospital Anxiety and Depression Scale (HADS) was used to assess symptoms of depression (HADS-DEP) and anxiety (HADS-ANX). RESULTS From baseline to 12 weeks, synbiotic supplementation resulted in a significant decrease in HADS-DEP score in a subgroup of patients with depressive symptom (HADS-DEP ≥ 8) compared to the placebo and probiotic supplementation (p = .001, p = .002, respectively) and in all patients compared to the placebo (p = .004). There was no significant difference among the groups in terms of HADS-ANX scores. However, the HADS-ANX scores decreased significantly in the synbiotic group compared to the baseline in all patients (p = .047) and also patients with depressive symptom (p = .03). In addition, in a subgroup of HD patients with depressive symptom, the serum BDNF increased significantly in the synbiotic group when compared to the placebo (p < .001) and probiotic group (p = .011). CONCLUSION Overall, 12 weeks of synbiotic supplementation resulted in greater improvement in depression symptoms and serum BDNF level compared to the probiotic supplementation in HD patients especially in the subgroup of patients with depression symptoms.
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Brain-Derived Neurotrophic Factor in Neonatal Seizures.
Sullivan, BJ, Kadam, SD
Pediatric neurology. 2021;:35-39
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Abstract
Brain-derived neurotrophic factor (BDNF), a member of the neurotrophin family, has an extensively studied classical role in neuronal growth, differentiation, survival, and plasticity. Neurotrophic, from the Greek neuro and trophos, roughly translates as "vital nutrition for the brain." During development, BDNF and its associated receptor tyrosine receptor kinase B are tightly regulated as they influence the formation and maturation of neuronal synapses. Preclinical research investigating the role of BDNF in neurological disorders has focused on the effects of decreased BDNF expression on the development and maintenance of neuronal synapses. In contrast, heightened BDNF-tyrosine receptor kinase B activity has received less scrutiny for its role in neurological disorders. Recent studies suggest that excessive BDNF-tyrosine receptor kinase B signaling in the developing brain may promote the hyperexcitability that underlies refractory neonatal seizures. This review will critically examine BDNF-tyrosine receptor kinase B signaling in the immature brain, its role in the emergence of refractory neonatal seizures, and the potential of targeting BDNF-TrkB signaling as a novel antiseizure strategy.