scholarly journals A peroxisome deficiency–induced reductive cytosol state up-regulates the brain-derived neurotrophic factor pathway

2020 ◽  
Vol 295 (16) ◽  
pp. 5321-5334 ◽  
Author(s):  
Yuichi Abe ◽  
Masanori Honsho ◽  
Ryoko Kawaguchi ◽  
Takashi Matsuzaki ◽  
Yayoi Ichiki ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Neurotrophic Factor ◽  
Hippocampal Neurons ◽  
Cell Communication ◽  
Brain Derived Neurotrophic Factor ◽  
Bdnf Expression ◽  
Multiple Organs ◽  
The Central Nervous System ◽  
And Function ◽  
The Brain

The peroxisome is a subcellular organelle that functions in essential metabolic pathways, including biosynthesis of plasmalogens, fatty acid β-oxidation of very-long-chain fatty acids, and degradation of hydrogen peroxide. Peroxisome biogenesis disorders (PBDs) manifest as severe dysfunction in multiple organs, including the central nervous system (CNS), but the pathogenic mechanisms in PBDs are largely unknown. Because CNS integrity is coordinately established and maintained by neural cell interactions, we here investigated whether cell-cell communication is impaired and responsible for the neurological defects associated with PBDs. Results from a noncontact co-culture system consisting of primary hippocampal neurons with glial cells revealed that a peroxisome-deficient astrocytic cell line secretes increased levels of brain-derived neurotrophic factor (BDNF), resulting in axonal branching of the neurons. Of note, the BDNF expression in astrocytes was not affected by defects in plasmalogen biosynthesis and peroxisomal fatty acid β-oxidation in the astrocytes. Instead, we found that cytosolic reductive states caused by a mislocalized catalase in the peroxisome-deficient cells induce the elevation in BDNF secretion. Our results suggest that peroxisome deficiency dysregulates neuronal axogenesis by causing a cytosolic reductive state in astrocytes. We conclude that astrocytic peroxisomes regulate BDNF expression and thereby support neuronal integrity and function.

scholarly journals Brain-Derived Neurotrophic Factor and Diabetes

2020 ◽  
Vol 21 (3) ◽  
pp. 841 ◽  
Author(s):  
Olga Rozanska ◽  
Aleksandra Uruska ◽  
Dorota Zozulinska-Ziolkiewicz
Keyword(s):  
Neurotrophic Factor ◽  
Brain Function ◽  
Clinical Problem ◽  
Brain Derived Neurotrophic Factor ◽  
Chronic Complications ◽  
Neuronal Tissue ◽  
Beneficial Impact ◽  
The Central Nervous System ◽  
And Function ◽  
Made In

Diabetes and its chronic complications still represent a great clinical problem, despite improvements made in the diagnosis and treatment of the disease. People with diabetes have a much higher risk of impaired brain function and psychiatric disorders. Neurotrophins are factors that protect neuronal tissue and improve the function of the central nervous system, and among them is brain-derived neurotrophic factor (BDNF). The level and function of BDNF in diabetes seems to be disturbed by and connected with the presence of insulin resistance. On the other hand, there is evidence for the highly beneficial impact of physical activity on brain function and BDNF level. However, it is not clear if this protective phenomenon works in the presence of diabetes. In this review, we summarize the current available research on this topic and find that the results of published studies are ambiguous.

scholarly journals Association between Obesity and Circulating Brain-Derived Neurotrophic Factor (BDNF) Levels: Systematic Review of Literature and Meta-Analysis

2018 ◽  
Vol 19 (8) ◽  
pp. 2281 ◽  
Author(s):  
Leonardo Sandrini ◽  
Alessandro Di Minno ◽  
Patrizia Amadio ◽  
Alessandro Ieraci ◽  
Elena Tremoli ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
Meta Analysis ◽  
Brain Derived Neurotrophic Factor ◽  
Obese Patients ◽  
Review Of Literature ◽  
Bdnf Expression ◽  
Subject Recruitment ◽  
And Storage ◽  
The Brain ◽  
Circulating Levels

Reduction in brain-derived neurotrophic factor (BDNF) expression in the brain as well as mutations in BDNF gene and/or of its receptor are associated to obesity in both human and animal models. However, the association between circulating levels of BDNF and obesity is still not defined. To answer this question, we performed a meta-analysis carrying out a systematic search in electronic databases. Ten studies (307 obese patients and 236 controls) were included in the analysis. Our data show that obese patients have levels of BDNF similar to those of controls (SMD: 0.01, 95% CI: −0.28, 0.30, p = 0.94). The lack of difference was further confirmed both in studies in which BDNF levels were assessed in serum (MD: −0.93 ng/mL, 95% CI: −3.34, 1.48, p = 0.45) and in plasma (MD: 0.15 ng/mL, 95% CI: −0.09, 0.39, p = 0.23). Data evaluation has shown that some bias might affect BDNF measurements (e.g., subject recruitment, procedures of sampling, handling, and storage), leading to a difficult interpretation of the results. Standardization of the procedures is still needed to reach strong, affordable, and reliable conclusions.

Glucocorticoids change the transcript levels of galanin, galanin receptor-2 and brain-derived neurotrophic factor in rat hippocampal neurons

2018 ◽  
Author(s):  
Fangyan Pan ◽  
Chengying Yang ◽  
Qing Xie ◽  
Yang Yang ◽  
Xianmei Luo ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
Hippocampal Neurons ◽  
Brain Derived Neurotrophic Factor ◽  
Control Group ◽  
High Concentration ◽  
Galanin Receptor ◽  
Mda Content ◽  
And Function ◽  
Hippocampal Structure ◽  
Transcription Expression

Glucocorticoids (GCs) can affect hippocampal structure and function in animals and humans. This study was designed to investigate the possible functional molecules and mechanisms involved in the action of GCs on hippocampal neurons. Rat primary hippocampal neurons were cultured and treated with glucocorticoids at a low concentration (LC, 10-8 mol/L), a middle concentration (MC, 10-7 mol/L) and a high concentration (HC, 10-6 mol/L). The results indicate that GCs do not change the viability of hippocampal neurons but do change the catalase (CAT) activity and malondialdehyde (MDA) content. The transcription expression levels of brain derived neurotrophic factor (BDNF), galanin (GAL), galanin receptor-2 (GALR2), and neuropeptide Y receptor-5 (NPYR5) genes in the HC group were significantly higher than those in the control group (p less than 0.05). These results suggest that hippocampal neurons launch the neuron protection pathways mediated by GAL, GALR2 and BDNF molecules when encountering an experimentally high concentration of corticosteroids.

Normal eye-specific patterning of retinal inputs to murine subcortical visual nuclei in the absence of brain-derived neurotrophic factor

2005 ◽  
Vol 22 (1) ◽  
pp. 27-36 ◽  
Author(s):  
ALVIN W. LYCKMAN ◽  
GUOPING FAN ◽  
MARIBEL RIOS ◽  
RUDOLF JAENISCH ◽  
MRIGANKA SUR
Keyword(s):  
Neurotrophic Factor ◽  
Germ Line ◽  
Brain Derived Neurotrophic Factor ◽  
Neural Systems ◽  
Bdnf Expression ◽  
Differential Survival ◽  
Visual Inputs ◽  
Conditional Mutant ◽  
The Central Nervous System ◽  
Dependent Growth

Brain-derived neurotrophic factor (BDNF) is a preferred ligand for a member of the tropomyosin-related receptor family, trkB. Activation of trkB is implicated in various activity-independent as well as activity-dependent growth processes in many developing and mature neural systems. In the subcortical visual system, where electrical activity has been implicated in normal development, both differential survival, as well as remodeling of axonal arbors, have been suggested to contribute to eye-specific segregation of retinal ganglion cell inputs. Here, we tested whether BDNF is required for eye-specific segregation of visual inputs to the lateral geniculate nucleus and the superior colliculus, and two other major subcortical target fields in mice. We report that eye-specific patterning is normal in two mutants that lack BDNF expression during the segregation period: a germ-line knockout for BDNF, and a conditional mutant in which BDNF expression is absent or greatly reduced in the central nervous system. We conclude that the availability of BDNF is not necessary for eye-specific segregation in subcortical visual nuclei.

scholarly journals Brain-derived neurotrophic factor as a potential therapeutic tool in the treatment of nervous system disorders

2020 ◽  
Vol 74 ◽  
pp. 517-531
Author(s):  
Wioletta Kazana ◽  
Agnieszka Zabłocka
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurotrophic Factor ◽  
Intracellular Transport ◽  
Brain Derived Neurotrophic Factor ◽  
Nerve Cells ◽  
The Body ◽  
Bdnf Level ◽  
The Central Nervous System ◽  
The Brain

Brain-derived neurotrophic factor (BDNF) plays an important role in the proper functioning of the nervous system. It regulates the growth and survival of nerve cells, and is crucial in processes related to the memory, learning and synaptic plasticity. Abnormalities related to the distribution and secretion of BDNF protein accompany many diseases of the nervous system, in the course of which a significant decrease in BDNF level in the brain is observed. Impairments of BDNF transport may occur, for example, in the event of a single nucleotide polymorphism in the Bdnf (Val66Met) coding gene or due to the dysfunctions of the proteins involved in intracellular transport, such as huntingtin (HTT), huntingtin-associated protein 1 (HAP1), carboxypeptidase E (CPE) or sortilin 1 (SORT1). One of the therapeutic goals in the treatment of diseases of the central nervous system may be the regulation of expression and secretion of BDNF protein by nerve cells. Potential therapeutic strategies are based on direct injection of the protein into the specific region of the brain, the use of viral vectors expressing the Bdnf gene, transplantation of BDNF-producing cells, the use of substances of natural origin that stimulate the cells of the central nervous system for BDNF production, or the use of molecules activating the main receptor for BDNF – tyrosine receptor kinase B (TrkB). In addition, an appropriate lifestyle that promotes physical activity helps to increase BDNF level in the body. This paper summarizes the current knowledge about the biological role of BDNF protein and proteins involved in intracellular transport of this neurotrophin. Moreover, it presents contemporary research trends to develop therapeutic methods, leading to an increase in the level of BDNF protein in the brain.

The brain-derived neurotrophic factor (BDNF) system as a therapeutical target for development of drugs restoring innervation

2017 ◽  
pp. 142-152
Author(s):  
Д.В. Стамбольский ◽  
О.С. Плеханова ◽  
И.Ю. Юдина ◽  
Н.И. Калинина ◽  
М.Н. Карагяур ◽  
...  
Keyword(s):  
Nervous System ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Current Data ◽  
Bdnf Expression ◽  
Promising Therapeutic Target ◽  
Nervous System Function ◽  
The Brain ◽  
Stimulation Of

Мозговой нейротрофический фактор (BDNF) является одним из основных нейротрофических факторов, участвующих в поддержании функционирования и регенерации нервной системы. В последние годы BDNF рассматривают как многообещающую терапевтическую мишень, на основании полученных данных о том, что BDNF улучшает регенерацию нейронов. Цель обзора - суммировать данные об экспрессии BDNF, его сигнализации, эффектах и механизмах стимуляции реиннервации. Анализ исследований последних десятилетий позволяет сделать заключение о целесообразности и перспективности разработок, направленных на создание лекарственных препаратов на основе BDNF для регенерации компонентов нервной системы. Brain-derived neurotrophic factor (BDNF) is a major neurotrophic factor maintaining the nervous system function and regeneration. Based on reports indicating that BDNF enhances neuronal regeneration, in recent years, BDNF has been considered a promising therapeutic target. The aim of this review was to summarize current data on BDNF expression, signaling, and mechanisms for stimulation of reinnervation. Conclusion. Recent studies of the role of BDNF showed that continuation of research and development of BDNF-based drugs stimulating regeneration of nervous system components is advisable and promising.

scholarly journals High intensity exercise increases brain derived neurotrophic factor expression and number of hippocampal neurons in rats

2020 ◽  
Vol 16 (4) ◽  
pp. 325-332
Author(s):  
A. Pranoto ◽  
E. Wahyudi ◽  
R.E. Prasetya ◽  
S. Fauziyah ◽  
R.G. Kinanti ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
High Intensity ◽  
Hippocampal Neurons ◽  
Brain Derived Neurotrophic Factor ◽  
High Intensity Exercise ◽  
Control Group ◽  
Pop Music ◽  
Bdnf Expression ◽  
Fast Tempo ◽  
Exercise Treadmill

The decrease in brain derived neurotrophic factor (BDNF) expression and number of hippocampal neurons are two indicators in the decrease of memory function, cognitive, and learning function. The present study aimed to determine BDNF expression and the number of hippocampal neurons on moderate and high intensity exercise by listening to music. Design of the present study was a randomised control group post-test only design. A total of 33 male rats, Rattus norvegicus strain Wistar, aged eight weeks, with body weight 160±20 g were randomly divided into three groups: Group 1 (G1) (n=11, control group without intervention), Group 2 (G2) (n=11, performed moderate intensity exercise, treadmill 14-16 m/min for 30 min by listening to pop music with fast tempo of 160 beats/min) and Group 3 (G3) (n=11, high intensity exercise, treadmill 22-25 m/min for 20 min by listening to pop music with fast tempo of 160 beats/min). The intervention was performed between 17:00-21:00 pm, three times per week for 12 weeks. Blood and brain samples were obtained and evaluated 12 h after the end of the last exercise. BDNF serum was measured using ELISA and hippocampal neurons were stained by haematoxylin-eosin and counted using OlyVIA software. Study results showed a BDNF for G1 of 1,098.14±135.31 pg/ml, G2 of 1,113.72±65.87 pg/ml, and G3 of 1,331.56±105.35 pg/ml (P=0.001). The total number of hippocampal neurons for G1 was 54.75±6.83 cells, for G2 59.87±7.68 cells, and G3 80.58±9.79 cells (P=0.001). According to the study it can be concluded that high intensity exercise combined by listening to music with a fast tempo of 160 beats/min increases BDNF expression and the number of hippocampal neurons.

scholarly journals An Overview of Brain-Derived Neurotrophic Factor and Implications for Excitotoxic Vulnerability in the Hippocampus

2011 ◽  
Vol 2011 ◽  
pp. 1-12 ◽  
Author(s):  
Patrick S. Murray ◽  
Philip V. Holmes
Keyword(s):  
Neurotrophic Factor ◽  
Hippocampal Formation ◽  
Brain Derived Neurotrophic Factor ◽  
Bdnf Expression ◽  
Endogenous Factors ◽  
Beneficial Effects ◽  
Highly Sensitive ◽  
Excitotoxic Damage ◽  
Exercise Induced ◽  
And Function

The present paper examines the nature and function of brain-derived neurotrophic factor (BDNF) in the hippocampal formation and the consequences of changes in its expression. The paper focuses on literature describing the role of BDNF in hippocampal development and neuroplasticity. BDNF expression is highly sensitive to developmental and environmental factors, and increased BDNF signaling enhances neurogenesis, neurite sprouting, electrophysiological activity, and other processes reflective of a general enhancement of hippocampal function. Such increases in activity may mediate beneficial effects such as enhanced learning and memory. However, the increased activity also comes at a cost: BDNF plasticity renders the hippocampus more vulnerable to hyperexcitability and/or excitotoxic damage. Exercise dramatically increases hippocampal BDNF levels and produces behavioral effects consistent with this phenomenon. In analyzing the literature regarding exercise-induced regulation of BDNF, this paper provides a theoretical model for how the potentially deleterious consequences of BDNF plasticity may be modulated by other endogenous factors. The peptide galanin may play such a role by regulating hippocampal excitability.

scholarly journals Environmental Enrichment Effects on the Brain-Derived Neurotrophic Factor Expression in Healthy Condition, Alzheimer’s Disease, and Other Neurodegenerative Disorders

2021 ◽  
pp. 1-18
Author(s):  
Debora Cutuli ◽  
Eugenia Landolfo ◽  
Laura Petrosini ◽  
Francesca Gelfo
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurotrophic Factor ◽  
Environmental Enrichment ◽  
Brain Plasticity ◽  
Regulation Of Gene Expression ◽  
Experimental Studies ◽  
Brain Derived Neurotrophic Factor ◽  
Bdnf Expression ◽  
The Brain

Brain-derived neurotrophic factor (BDNF), a protein belonging to the neurotrophin family, is known to be heavily involved in synaptic plasticity processes that support brain development, post-lesion regeneration, and cognitive performances, such as learning and memory. Evidence indicates that BDNF expression can be epigenetically regulated by environmental stimuli and thus can mediate the experience-dependent brain plasticity. Environmental enrichment (EE), an experimental paradigm based on the exposure to complex stimulations, constitutes an efficient means to investigate the effects of high-level experience on behavior, cognitive processes, and neurobiological correlates, as the BDNF expression. In fact, BDNF exerts a key role in mediating and promoting EE-induced plastic changes and functional improvements in healthy and pathological conditions. This review is specifically aimed at providing an updated framework of the available evidence on the EE effects on brain and serum BDNF levels, by taking into account both changes in protein expression and regulation of gene expression. A further purpose of the present review is analyzing the potential of BDNF regulation in coping with neurodegenerative processes characterizing Alzheimer’s disease (AD), given BDNF expression alterations are described in AD patients. Moreover, attention is also paid to EE effects on BDNF expression in other neurodegenerative disease. To investigate such a topic, evidence provided by experimental studies is considered. A deeper understanding of environmental ability in modulating BDNF expression in the brain may be fundamental in designing more tuned and effective applications of complex environmental stimulations as managing approaches to AD.

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