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Journal articles on the topic 'Brain-derived neurotropic factor'

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Author: Grafiati

Published: 10 December 2022

Last updated: 29 January 2023

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1

Ibrahim, Abdallah Mohammad, Lalita Chauhan, Aditi Bhardwaj, Anjali Sharma, Faizana Fayaz, Bhumika Kumar, Mohamed Alhashmi, Noora AlHajri, Md Sabir Alam, and Faheem Hyder Pottoo. "Brain-Derived Neurotropic Factor in Neurodegenerative Disorders." Biomedicines 10, no. 5 (May 16, 2022): 1143. http://dx.doi.org/10.3390/biomedicines10051143.

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Globally, neurodegenerative diseases cause a significant degree of disability and distress. Brain-derived neurotrophic factor (BDNF), primarily found in the brain, has a substantial role in the development and maintenance of various nerve roles and is associated with the family of neurotrophins, including neuronal growth factor (NGF), neurotrophin-3 (NT-3) and neurotrophin-4/5 (NT-4/5). BDNF has affinity with tropomyosin receptor kinase B (TrKB), which is found in the brain in large amounts and is expressed in several cells. Several studies have shown that decrease in BDNF causes an imbalance in neuronal functioning and survival. Moreover, BDNF has several important roles, such as improving synaptic plasticity and contributing to long-lasting memory formation. BDNF has been linked to the pathology of the most common neurodegenerative disorders, such as Alzheimer’s and Parkinson’s disease. This review aims to describe recent efforts to understand the connection between the level of BDNF and neurodegenerative diseases. Several studies have shown that a high level of BDNF is associated with a lower risk for developing a neurodegenerative disease.

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2

Pandit, Mahashweta, Tapan Behl, Monika Sachdeva, and Sandeep Arora. "Role of brain derived neurotropic factor in obesity." Obesity Medicine 17 (March 2020): 100189. http://dx.doi.org/10.1016/j.obmed.2020.100189.

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3

Buckley, Peter F., Anilkumar Pillai, Denise Evans, Edna Stirewalt, and Sahebarao Mahadik. "Brain derived neurotropic factor in first-episode psychosis." Schizophrenia Research 91, no. 1-3 (March 2007): 1–5. http://dx.doi.org/10.1016/j.schres.2006.12.026.

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4

Lee, Eugine, Yeon Ik Jeong, Seon Mi Park, Jong Yun Lee, Ji Hye Kim, Sun Woo Park, M. S. Hossein, et al. "Beneficial effects of brain-derived neurotropic factor on in vitro maturation of porcine oocytes." Reproduction 134, no. 3 (September 2007): 405–14. http://dx.doi.org/10.1530/rep-06-0288.

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In an effort to improve the quality ofin vitroproduced porcine embryos, we investigated the effect of brain-derived neurotropic factor (BDNF), a neurotropin family member, onin vitromaturation (IVM) of porcine oocytes. The expression of BDNF and truncated isoforms of its receptor, tyrosine kinase B (TrkB), and p75 common neurotropin receptor was detected in both follicular cells and metaphase-I stage oocytes by RT-PCR. However, mRNA of full-length TrkB was not found in oocytes although it was detected in follicular cells. The expression pattern of BDNF and TrkB was confirmed by immunohistochemistry. Supplementation with BDNF (30 ng/ml) during IVM significantly (P< 0.05) increased the first polar body extrusion and glutathione levels in oocytes, whereas the effect of BDNF on nuclear maturation was diminished when gonadotropin and epidermal growth factor (EGF) were added to the culture media. However, treatment with BDNF (30 ng/ml) along with EGF (10 ng/ml) in the presence of gonadotropin significantly (P< 0.05) increased the developmental competence of oocytes to the blastocyst stage after bothin vitrofertilization (IVF; 29.1% when compared with control, 15.6%) and somatic cell nuclear transfer (SCNT; 13.6% when compared with control, 3%). This appeared to reflect a stimulatory interaction between BDNF and EGF to enhance the cytoplasmic maturation of oocytes to support successful preimplantation development. In conclusion, BDNFenhanced nuclearand cytoplasmic maturation of oocytes by autocrine and/or paracrine signals. Also, when used together with EGF, BDNF increased the developmental potency of embryos after IVF and SCNT, demonstrating an improvedin vitroproduction protocol for porcine oocytes.

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5

Yang, Miyoung, Changjong Moon, Jinwook Kim, Sueun Lee, Sohi Kang, Sung-Ho Kim, and Jong-Choon Kim. "Brain-derived neurotropic factor and GABAergic transmission in neurodegeneration and neuroregeneration." Neural Regeneration Research 12, no. 10 (2017): 1733. http://dx.doi.org/10.4103/1673-5374.217353.

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Sedlacek, Carly, Ryan T. Wiet, Emily C. Tagesen, Eliott Arroyo, Ellen L. Glickman, and Adam R. Jajtner. "Brain Derived Neurotropic Factor Response To Aerobic Exercise In The Cold." Medicine & Science in Sports & Exercise 52, no. 7S (July 2020): 771. http://dx.doi.org/10.1249/01.mss.0000683604.90282.6d.

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7

Stranahan, Alexis M., Thiruma V. Arumugam, and Mark P. Mattson. "Lowering Corticosterone Levels Reinstates Hippocampal Brain-Derived Neurotropic Factor and Trkb Expression without Influencing Deficits in Hypothalamic Brain-Derived Neurotropic Factor Expression in Leptin Receptor-Deficient Mice." Neuroendocrinology 93, no. 1 (2011): 58–64. http://dx.doi.org/10.1159/000322808.

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8

Hidayat, Andri, Mansyur Arief, Andi Wijaya, and Suryani As'ad. "Vascular Endothelial Growth Factor and Brain-Derived Neurotropic Factor Levels in Ischemic Stroke Subject." Indonesian Biomedical Journal 8, no. 2 (August 1, 2016): 115. http://dx.doi.org/10.18585/inabj.v8i2.206.

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BACKGROUND: Vascular endothelial growth factor (VEGF) and brain-derived neurotropic factor (BDNF) present during early neuronal development and play important roles in the process of neurorepairing includes angiogenesis, neurogenesis and neuronal plasticity after ischemic stroke. In this study, we observed VEGF and BDNF levels of subjects with ischemic stroke in different onset time.METHODS: A cross sectional study was designed. Study subjects were 51 ischemic stroke subjects, aged 30-80 years old, recruited from Gatot Subroto Army Central Hospital, Jakarta, Indonesia. Ischemic stroke was diagnosed by neurologist, based on clinical examination and magnetic resonance imaging (MRI) result. Subjects were divided into 3 groups based on onset time of stroke: <7 days (group A), 7-30 days (group B) and >30 days (Group C). VEGF and BDNF levels from serum were measured using lumine Magpix. The data was analyzed for comparison and correlation.RESULTS: VEGF and BDNF levels of group B and C were significantly different with p=0.034 and p=0.007, respectively. Group B had the highest VEGF levels, whereas Group C had the highest BDNF level. VEGF and BDNF levels in each group were not significantly correlated.CONCLUSION: Each stage of time after ischemic stroke has different recovery activities like angiogenesis, neurogenesis and plasticity. Angiogenesis process was optimum in 7-30 days after onset. in more than 30 days onset, Low VEGF with high BDNF have important role in a long period of time after the onset of stroke in the regeneration and repair, such as maintaining neuronal survival and plasticity.KEYWORDS: ischemic stroke, VEGF, BDNF

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9

Mishchenko, T. A., M. V. Vedunova, E. V. Mitroshina, A. S. Pimashkin, and I. V. Mukhina. "Neurotropic Effect of Brain-Derived Neurotrophic Factor at Different Stages of Dissociated Hippocampal Cultures Development in vitro." Sovremennye tehnologii v medicine 7, no. 3 (September 2015): 47–54. http://dx.doi.org/10.17691/stm2015.7.3.06.

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Mohan, Nithyakalyani, and Anusha Sunder. "A comprehensive evaluation of brain derived neurotropic growth factor gene on Bharatnatyam dancers." Precision Medicine Research 4, no. 2 (2022): 6. http://dx.doi.org/10.53388/pmr20220006.

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Şimşek, Şeref, Salih Gençoğlan, Tuğba Yüksel, İbrahim Kaplan, and Hüseyin Aktaş. "Lower Brain-Derived Neurotropic Factor Levels in Untreated Adolescents With First-Episode Psychosis." Journal of Clinical Psychopharmacology 35, no. 5 (October 2015): 596–99. http://dx.doi.org/10.1097/jcp.0000000000000378.

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Peng, J. Y., X. P. An, F. Fang, K. X. Gao, H. Y. Xin, P. Han, L. J. Bao, H. D. Ma, and B. Y. Cao. "MicroRNA-10b suppresses goat granulosa cell proliferation by targeting brain-derived neurotropic factor." Domestic Animal Endocrinology 54 (January 2016): 60–67. http://dx.doi.org/10.1016/j.domaniend.2015.09.005.

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Widodo, Joko, Andi Asadul, Andi Wijaya, and Gatot Lawrence. "Correlation between Nerve Growth Factor (NGF) with Brain Derived Neurotropic Factor (BDNF) in Ischemic Stroke Patient." Bali Medical Journal 5, no. 2 (May 3, 2016): 10. http://dx.doi.org/10.15562/bmj.v5i2.199.

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Humińska-Lisowska, Kinga, Jolanta Chmielowiec, Krzysztof Chmielowiec, Marta Niewczas, Milena Lachowicz, Paweł Cięszczyk, Jolanta Masiak, et al. "Associations of Brain-Derived Neurotropic Factor rs6265 Gene Polymorphism with Personality Dimensions among Athletes." International Journal of Environmental Research and Public Health 19, no. 15 (August 7, 2022): 9732. http://dx.doi.org/10.3390/ijerph19159732.

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Brain-Derived Neurotropic Factor (BDNF) is one of the essential mediating factors of exercise-induced neuroplasticity, but the underlying molecular mechanisms of exercise-induced neuroplasticity are still largely unknown. Personality dimensions differentiate individuals and depend on genes and environmental factors. The dimensions of openness to experience, emotional stability, extraversion and conscientiousness have been reported to be positively related to performance; considering agreeableness, a negative relation with sports performance was emphasized. However, not enough effort has been put into investigating the relationship between genetic polymorphisms affecting psychological abilities and competitive power sports. The aim of this study was to investigate the association of the rs6265 polymorphism of BDNF with personality dimensions in martial arts athletes. The study was conducted among martial arts athletes. The study group included 258 volunteers (martial arts athletes (n = 106) and controls (n = 152). BDNF polymorphism testing was performed using the real-time PCR method; personality dimensions were assessed using standardized NEO-FFI questionnaires. All analyses were performed using STATISTICA 13. We observed that martial arts athletes’ G/G genotypes compared to the control group G/G genotypes presented significantly higher severity of personality dimension “conscientiousness”. In comparison with the controls, the case group subjects had significantly higher scores in the dimension extraversion (M 6.89 vs. M 6.43, p = 0.0405) and conscientiousness/scale (M 7.23 vs. M 5.89, p < 0.0001). The results of 2 × 3 factorial ANOVA noticed a statistically significant effect of combined factor BDNF rs6265 genotype of martial arts/control (F2,252 = 3.11, p = 0.0465, η2 = 0.024). Additionally, we observed that the results of 2 × 3 factorial ANOVA showed a statistically significant influence of combined factor BDNF rs6265 of genotype martial arts/ control (F2,252 = 6.16, p = 0.0024, η2 = 0.047). The combination of the analysis of personality dimensions with genetics—as in the case of the polymorphism of the BDNF gene related to neuroplasticity—indicates that neurobiology cannot be ignored in educating sports champions. We already know that this is related to genetics. However, little is still known about the influence of personality traits on sports performance. We observed that martial arts athletes’ G/G genotypes, in comparison to the control group’s G/G genotypes, presented significantly higher severity of personality dimension “conscientiousness”. This is worthy of further analysis and probably longitudinal studies on a more numerous group of athletes.

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Ratnawati, Retty, Annisa Nurul Arofah, Anastasia Novitasari, Sartika Dewi Utami, Made Ayu Hariningsih, Masruroh Rahayu, Sri Budhi Rianawati, Hari Purnomo, and Mochammad Dalhar. "Catechins decrease neurological severity score through apoptosis and neurotropic factor pathway in rat traumatic brain injury." Universa Medicina 36, no. 2 (August 9, 2017): 110. http://dx.doi.org/10.18051/univmed.2017.v36.110-122.

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<p>BACKGROUND<br />Catechins inhibits apoptosis through anti oxidant and anti inflamation pathway. Catechins also increases brain-derived neurotrophic factor (BDNF). There was a few research that explained the role of catechins in traumatic brain injury (TBI). The objective of the study was to evaluate the effect of catechins administration on neurologic severity score (NSS) through apoptosis and neurotropic pathway in traumatic brain injury rat model.</p><p>METHODS<br />A post test only controlled group design was performed using traumatic brain injury rat (Rattus novergicus) model through weight drop models. It was devided into negative control group, positive control group, TBI+catechins 513 mg/kgBW, TBI+catechins 926 mg/kgBW, TBI+catechins 1113 mg/kgBW. NSS was measured in the first hours, day three, and day seven. The expressions of NFkB, TNFa, Bcl-2, Bax, caspase 3, caspase 8, BDNF, and the numbers of apoptosis cells were evaluated by imunohistochemystry method. One way Anova and Kruskal Wwallis were used to analyse the data.</p><p>Results <br />TNFa, caspase 8, number of apoptosis cells were significantly decreased on the seventh day administration compared to the third day administration (p<0.05). Catechins increased the expression of Bcl-2/Bax and BDNF significantly (p<0.05). Yet, there were no significant differences between expression of caspase 3, NSS, Bcl-2/Bax ratio, and BDNF toward third days administration of catechins compared with seven days administration (p>0.050).</p><p>Conclusions<br />Administration of catechins decreased NSS through inhibiting inflammation and apoptosis, as well as induced the neurotrophic factors in rat brain injury. Catechins may serve as a potential intervention for TBI.</p>

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Pillai, Anilkumar. "Brain-Derived Neurotropic Factor/TrkB Signaling in the Pathogenesis and Novel Pharmacotherapy of Schizophrenia." Neurosignals 16, no. 2-3 (2008): 183–93. http://dx.doi.org/10.1159/000111562.

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17

Smith, M. A., S. Makino, S. Y. Kim, and R. Kvetnansky. "Stress increases brain-derived neurotropic factor messenger ribonucleic acid in the hypothalamus and pituitary." Endocrinology 136, no. 9 (September 1995): 3743–50. http://dx.doi.org/10.1210/endo.136.9.7649080.

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Antunes-Lopes, T., R. Pinto, S. Carvalho-Barros, P. Diniz, C. Duarte-Cruz, C. Martins-Silva, and F. Cruz. "UP-03.200 Brain-Derived Neurotropic Factor: A New Potential Biomarker of Overactive Bladder Syndrome." Urology 78, no. 3 (September 2011): S411. http://dx.doi.org/10.1016/j.urology.2011.07.1288.

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19

Hargett, Tori D., Ryan T. Wiet, Elliot Arroyo, Emily C. Tagesen, Ellen L. Glickman, and Adam R. Jajtner. "Effect Of Heat On Serum And Plasma Brain-derived Neurotropic Factor During Aerobic Exercise." Medicine & Science in Sports & Exercise 52, no. 7S (July 2020): 972. http://dx.doi.org/10.1249/01.mss.0000686140.49719.b2.

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Gipson, Stephanie D., Shiloah A. Kviatkovsky, Adrian P. Othon, Alex O. Klemp, Jeong-Su Kim, and Michael J. Ormsbee. "Circulating Brain Derived Neurotropic Factor (BDNF) In Response To Three-day Ultra-endurance Racing." Medicine & Science in Sports & Exercise 52, no. 7S (July 2020): 1037. http://dx.doi.org/10.1249/01.mss.0000686864.51565.bd.

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21

Wang, Sheng-Yu, Michelle R. Freeman, Venkatachalem Sathish, Michael A. Thompson, Christina M. Pabelick, and Y. S. Prakash. "Sex Steroids Influence Brain-Derived Neurotropic Factor Secretion From Human Airway Smooth Muscle Cells." Journal of Cellular Physiology 231, no. 7 (November 26, 2015): 1586–92. http://dx.doi.org/10.1002/jcp.25254.

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Dhiman, Pooja, Aishwarya Say, Soundravally Rajendiren, Shivanand Kattimani, and Haritha Sagili. "Association of foetal APGAR and maternal brain derived neurotropic factor levels in postpartum depression." Asian Journal of Psychiatry 11 (October 2014): 82–83. http://dx.doi.org/10.1016/j.ajp.2014.06.022.

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Tanure, Marco Túlio A., Rodrigo S. Gomez, Rubens Carlos L. Hurtado, Antônio L. Teixeira, and Renan Barros Domingues. "Increased serum levels of brain-derived neurotropic factor during migraine attacks: a pilot study." Journal of Headache and Pain 11, no. 5 (June 17, 2010): 427–30. http://dx.doi.org/10.1007/s10194-010-0233-0.

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Cho, Su-Youn, and Hee-Tae Roh. "Effects of Exercise Training on Neurotrophic Factors and Blood–Brain Barrier Permeability in Young-Old and Old-Old Women." International Journal of Environmental Research and Public Health 19, no. 24 (December 16, 2022): 16896. http://dx.doi.org/10.3390/ijerph192416896.

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Aging and regular exercise may have opposite effects on brain health, and although oxidative stress and sirtuins may be involved in these effects, studies on this topic are limited. Accordingly, the present study aimed to verify the effect of exercise training on oxidant–antioxidant balance, neurotrophic factors, blood–brain barrier permeability, and sirtuins in young-old and old-old women. The study participants were 12 women aged 65–74 years (Young-Old group) and 12 women aged 75–84 years (Old-Old group). All of the selected participants performed exercise training consisting of treadmill walking and resistance band exercise three times a week for 12 weeks. Blood samples were collected before and after exercise training to analyze serum oxidant–antioxidant markers (reactive oxygen species [ROS], superoxide dismutase [SOD]), neurotrophic factor (brain-derived neurotrophic factor [BDNF], vascular endothelial growth factor [VEGF]) levels, and blood–brain barrier permeability marker (S100 calcium-binding protein β [S100β], matrix metalloproteinase-9 [MMP-9]) levels, and sirtuin (SIRT-1, SIRT-2, SIRT-3) levels. The Young-Old group showed significantly increased SOD, BDNF, VEGF, SIRT-1, and SIRT-3 levels after training in comparison with the levels before training (p < 0.05), and a significantly higher BDNF level than the Old-Old group after training (p < 0.05). On the other hand, the Old-Old group showed significantly higher SIRT-1 levels after training in comparison with the levels before training (p < 0.05). Thus, exercise training may be effective in increasing the levels of neurotropic factors and reducing blood–brain barrier permeability in the elderly women, and increased antioxidant capacity and elevated levels of sirtuins are believed to play a major role in these effects. The positive effect of exercise may be greater in participants of relatively young age.

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Frias, B., F. Cruz, and C. D. Cruz. "826 NERVE GROWTH FACTOR (NGF) AND BRAIN DERIVED NEUROTROPIC FACTOR (BDNF) PLAY COMPLEMENTARY ROLES IN BLADDER CONTROL." European Urology Supplements 10, no. 2 (March 2011): 261. http://dx.doi.org/10.1016/s1569-9056(11)60812-9.

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Mardiah, Ainal, Arni Amir, Andi Friadi, and Ellyza Nasrul. "Perbedaan Kadar Brain Derived Neurotropic Factor Neonatus Dari Ibu Hamil Normal Dan Anemia Defisiensi Besi." Jurnal Endurance 3, no. 3 (October 25, 2018): 568. http://dx.doi.org/10.22216/jen.v3i3.3706.

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<p><em>Iron deficiency anemia is anemia caused by iron deficiency in the blood. Maternal iron deficiency affects the low iron reserves in neonates </em><em>and it also influences on </em><em>Brain Derived Neurotropic Factor (BDNF) </em><em> which affects cognitive function.</em><em> </em><em>The purpose of this study was to determine the difference mean of BDNF in neonates from normal pregnant women and pregnant women with iron deficiency. </em><em>The design of this research was Cross Sectional</em><em> </em><em>design. This research was conducted in Community Health Center of Lubuk Buaya, Ambacang Community Health Center, Community Health Center of Ikur Koto Health Center and Biomedical Laboratory of Andalas University on February 2017 to April 2018. There were 42 pregnant women was selected as sample e of this research. The samples were chosen by Consecutive Sampling. Then, the sample is divided into two groups: normal pregnant women and pregnant women with iron deficiency anemia. BDNF are examined by the ELISA. Next, the data were analyzed by using T test. The levels of BDNF neonates in normal pregnant group was 3.65(ng/ml) and the anemia pregnant group was 1.74(ng/ml) (p <0.05). There was significant difference of BDNF levels in neonates from normal pregnant women and pregnant women with iron deficiency anemia. </em><em>The conclusion of this study is there is a difference of average BDNF in neonates from normal pregnant women and pregnant women with iron deficiency.</em></p><p> </p><p>Anemia defisiensi besi adalah anemia yang disebabkan karena kekurangan zat besi dalam darah. Defisiensi besi maternal berdampak pada rendahnya cadangan besi pada neonatus dan berdampak terhadap ekspresi Brain Derived Neurotropic Factor (BDNF) yang berpengaruh pada fungsi kognitif. Tujuan penelitian ini adalah untuk mengetahui perbedaan rerata kadar BDNF pada neonatus dari ibu hamil normal dan ibu hamil defisiensi besi. Desain penelitian ini adalah Cross Sectional. Penelitian dilakukan di Puskesmas Lubuk Buaya, Puskesmas Ambacang, Puskesmas Ikur Koto dan Laboratorium Biomedik Universitas Andalas pada bulan Februari 2017 – Juli 2018. Sampel Penelitian adalah ibu hamil sebanyak 42 orang yang dipilih secara Consecutive Sampling, sampel dibagi menjadi dua kelompok yaitu ibu hamil normal dan ibu hamil anemia defisiensi besi. BDNF diperiksa dengan metode ELISA. Data dianalisa menggunakan uji T test. Kadar BDNF neonatus pada ibu kelompok normal adalah 3,65(ng/ml) dan kelompok ibu anemia adalah 1,74(ng/ml) (p<0,05). Terdapat perbedaan bermakna kadar BDNF pada neonatus dari ibu hamil normal dan ibu anemia defisiensi besi. <em></em></p>

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Bercik, Premysl, Emmanuel Denou, Josh Collins, Wendy Jackson, Jun Lu, Jennifer Jury, Yikang Deng, et al. "The Intestinal Microbiota Affect Central Levels of Brain-Derived Neurotropic Factor and Behavior in Mice." Gastroenterology 141, no. 2 (August 2011): 599–609. http://dx.doi.org/10.1053/j.gastro.2011.04.052.

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de Krom, M., J. Hillebrand, J. Hendriks, A. van Elburg, and R. Adan. "P.1.19 The role of brain derived neurotropic factor (BDNF) in anorexia nervosa and hyperactivity." European Neuropsychopharmacology 15 (January 2005): S16—S17. http://dx.doi.org/10.1016/s0924-977x(05)80124-5.

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Pinnock, Scarlett B., and Joe Herbert. "Brain-derived neurotropic factor and neurogenesis in the adult rat dentate gyrus: interactions with corticosterone." European Journal of Neuroscience 27, no. 10 (May 2008): 2493–500. http://dx.doi.org/10.1111/j.1460-9568.2008.06250.x.

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Ney, Luke, Kim Felmingham, David S. Nichols, and Allison Matthews. "Brain-derived neurotropic factor and cortisol levels negatively predict working memory performance in healthy males." Neurobiology of Learning and Memory 175 (November 2020): 107308. http://dx.doi.org/10.1016/j.nlm.2020.107308.

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Kim, SJ, HJ Lee, YJ Lee, IH Cho, J. Shin, and SJ Cho. "The brain-derived neurotropic factor Val66Met polymorphism and cingulate gray matter volume in healthy Koreans." NeuroImage 47 (July 2009): S139. http://dx.doi.org/10.1016/s1053-8119(09)71379-5.

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Benedek, Kálmán. "Kinetics of recombinant human brain-derived neurotropic factor unfolding under reversed-phase liquid chromatography conditions." Journal of Chromatography A 646, no. 1 (August 1993): 91–98. http://dx.doi.org/10.1016/s0021-9673(99)87010-1.

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Fukushima, Arata, Shintaro Kinugawa, Tsuneaki Homma, Yoshihiro Masaki, Takaaki Furihata, Takashi Yokota, Shouji Matsushima, et al. "Serum Brain-Derived Neurotropic Factor Level Predicts Adverse Clinical Outcomes in Patients With Heart Failure." Journal of Cardiac Failure 21, no. 4 (April 2015): 300–306. http://dx.doi.org/10.1016/j.cardfail.2015.01.003.

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Lee, Jonghun, Nancy Laurin, Jennifer Crosbie, Abel Ickowicz, Tejaswee Pathare, Molly Malone, Rosemary Tannock, James L. Kennedy, Russell Schachar, and Cathy L. Barr. "Association study of the brain-derived neurotropic factor (BDNF) gene in attention deficit hyperactivity disorder." American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 144B, no. 8 (2007): 976–81. http://dx.doi.org/10.1002/ajmg.b.30437.

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Aliomrani, Mehdi, Azadeh Mesripour, and Tannaz Daneshseta. "Involvement of Mice Hippocampus Brain-derived Neurotrophic Factor in Diazinon-induced Depressive Behavior in Mice." Iranian Journal of Toxicology 16, no. 2 (April 1, 2022): 125–34. http://dx.doi.org/10.32598/ijt.16.2.902.1.

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Background: Diazinon (Dzn), an Organophosphorus (OP) pesticide, is extensively used in agriculture. Acetylcholinesterase inhibition is linked to OP toxicity, and there are major mental health concerns associated with the use of pesticides. The objective of this study was to assess the depressive behavior in an animal model following their exposure to Dzn and the effect on the Brain-Derived Neurotrophic Factor (BDNF) as a critical neurotropic factor. Methods: Male Swiss mice (N=42; 25±3g each) were used and their behaviors were eamined on including the locomotor, Forced Swimming (FST), and Sucrose Preference (SP) tests. These tests were performed the day after a single daily Dzn administration by gavage (2.5-20 mg/kg). Specific animal groups were exposed to Dzn daily (2.5-10 mg/kg) for 14 days, and a test was performed on days 7 and 15. Results: Following the acute exposure to Dzn, the animals’ locomotor activity did not change significantly. During the FST, Dzn at 20 mg/kg significantly increased the animals’ immobility time, indicating despair behavior. Imipramine, injected intraperitoneally at 10 mg/kg, did not cause the depressive behavior. The subacute exposure to Dzn induced less locomotor activity than that of the controls. The 7-day exposure to Dzn at 10 mg/kg significantly prolonged the immobility period compared to that of the controls. The 14-day Dzn exposure at 2.5, 5, or 10 mg/kg increased the immobility time significantly compared to that of the controls. None of the treatment groups showed SP, clearly showing animal anhedonia. The BDNF levels significantly decreased not only by subacute exposures to Dzn but also following a single exposure to this this pesticide. Conclusion: The acute and subacute exposure to Dzn induced depressive behavior and increased the BDNF levels in the hippocampus of Swiss male mice following exposure to Dzn at varying doses of 2.5, 5, or 10 mg/kg.

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Almeida, Felipe Borges, Helena Maria Tannhauser Barros, and Graziano Pinna. "Neurosteroids and Neurotrophic Factors: What Is Their Promise as Biomarkers for Major Depression and PTSD?" International Journal of Molecular Sciences 22, no. 4 (February 10, 2021): 1758. http://dx.doi.org/10.3390/ijms22041758.

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Even though major depressive disorder (MDD) and post-traumatic stress disorder (PTSD) are among the most prevalent and incapacitating mental illnesses in the world, their diagnosis still relies solely on the characterization of subjective symptoms (many of which are shared by multiple disorders) self-reported by patients. Thus, the need for objective measures that aid in the detection of and differentiation between psychiatric disorders becomes urgent. In this paper, we explore the potential of neurosteroids and neurotrophic proteins as biomarkers for MDD and PTSD. Circulating levels of the GABAergic neuroactive steroid, allopregnanolone, are diminished in MDD and PTSD patients, which corroborates the finding of depleted neurosteroid levels observed in animal models of these disorders. The neurotrophic protein, brain-derived neurotropic factor (BDNF), is also reduced in the periphery and in the brain of MDD patients and depressed-like animals that express lower neurosteroid levels. Although the role of BDNF in PTSD psychopathology seems less clear and merits more research, we propose a causal link between allopregnanolone levels and BDNF expression that could function as a biomarker axis for the diagnosis of both MDD and PTSD.

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Tsotsoros, Cindy, Madison Stout, and Misty Hawkins. "Associations of Adverse Childhood Experiences with Executive Function and Brain-Derived Neurotrophic Factor." Innovation in Aging 5, Supplement_1 (December 1, 2021): 1026. http://dx.doi.org/10.1093/geroni/igab046.3671.

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Abstract Adverse childhood experiences (ACEs) may predict markers of neurocognitive performance (i.e., executive function; EF) and brain health/plasticity (i.e., brain-derived neurotropic factor; BDNF). This pilot examined the magnitude of effects between: 1) ACES and EF performance, 2) ACEs and BDNF levels, and 3) EF performance and BDNF levels. We hypothesize that higher ACEs will be associated with poorer EF scores and lower BNDF levels and that lower EF scores will be associated with lower BDNF levels. Given the pilot nature of the study, an emphasis is placed on effect size vs. significance. Participants were 36 middle-aged women enrolled in the NICE SPACES trial (age=31.4 years, BMI=34.2, racially minoritized=37.9%). ACES were quantified using the 10-item Adverse Childhood Experiences Scale. EF was measured using the fluid cognition composite from the NIH Toolbox – Cognition Battery. BDNF was estimated using proBDNF levels estimated from serum collected via venipuncture. Higher ACEs levels were not directly associated with EF scores (b = 0.03, p = .854); but did show a meaningful negative beta coefficient with BDNF levels (b = -0.34, p = .053). EF scores and BDNF showed a positive coefficient that did not reach significance (b = .26, p = .122). In a modest pilot of middle-age women, higher ACEs were associated with lower BDNF, indicating greater adversity in childhood is linked to lower neurotrophins levels in adulthood. The lower BDNF levels may help explain poorer performance on cognitive tasks. Larger follow-up studies in more powered samples are warranted given the size of detected coefficients.

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Brigadski, T., and V. Leßmann. "BDNF: a regulator of learning and memory processes with clinical potential." e-Neuroforum 20, no. 1 (January 1, 2014): 1–11. http://dx.doi.org/10.1515/s13295-014-0053-9.

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AbstractMemories are believed to be represented by facilitated synaptic transmission of electrical signals in neuronal networks. The ability to acquire new memories or to change old memory content results from the plastic properties of the brain. Molecular changes in synaptic plasticity of neuronal networks are considered to be the cellular correlates of learning and memory, and the neurotrophin brain-derived neurotropic factor (BDNF) plays an important role in these processes. This neurotrophic factor coordinates a multitude of biological functions. In addition to its role in neuronal plasticity processes, such as long-term potentiation of synaptic transmission, the protein regulates the differentiation of neuronal precursor cells, synaptogenesis, and neuronal survival. Cellular processes like BDNF protein processing, anterograde and retrograde transport, as well as exocytosis and endocytosis of BDNF vesicles are necessary to enable the protein to fulfill its neuroprotective and plasticity-related functions in its target areas. Therefore, deficits in one of these functions, resulting in a reduction or a lack of BDNF supply, can result in dysfunctional or reduced synaptic plasticity in virtually every brain area. Since cognitive processes and mental health require the intact formation and modification of memory traces, a change in BDNF turnover is considered as a contributing factor to a number of neurodegenerative and psychological disorders. This review summarizes the current knowledge regarding the connection between BDNF, its role in synaptic plasticity and its role in brain.

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Kackley, Madison L., Alex Buga, Chris D. Crabtree, Teryn N. Sapper, Craig A. McElroy, Brian C. Focht, William J. Kraemer, and Jeff S. Volek. "Influence of Nutritional Ketosis Achieved through Various Methods on Plasma Concentrations of Brain Derived Neurotropic Factor." Brain Sciences 12, no. 9 (August 27, 2022): 1143. http://dx.doi.org/10.3390/brainsci12091143.

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Brain-Derived Neurotropic Factor (BDNF) expression is decreased in conditions associated with cognitive decline as well as metabolic diseases. One potential strategy to improve metabolic health and elevate BDNF is by increasing circulating ketones. Beta-Hydroxybutyrate (BHB) stimulates BDNF expression, but the association of circulating BHB and plasma BDNF in humans has not been widely studied. Here, we present results from three studies that evaluated how various methods of inducing ketosis influenced plasma BDNF in humans. Study 1 determined BDNF responses to a single bout of high-intensity cycling after ingestion of a dose of ketone salts in a group of healthy adults who were habitually consuming either a mixed diet or a ketogenic diet. Study 2 compared how a ketogenic diet versus a mixed diet impacts BDNF levels during a 12-week resistance training program in healthy adults. Study 3 examined the effects of a controlled hypocaloric ketogenic diet, with and without daily use of a ketone-salt, on BDNF levels in overweight/obese adults. We found that (1) fasting plasma BDNF concentrations were lower in keto-adapted versus non keto-adapted individuals, (2) intense cycling exercise was a strong stimulus to rapidly increase plasma BDNF independent of ketosis, and (3) clinically significant weight loss was a strong stimulus to decrease fasting plasma BDNF independent of diet composition or level of ketosis. These results highlight the plasticity of plasma BDNF in response to lifestyle factors but does not support a strong association with temporally matched BHB concentrations.

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Bouakkar, Jenan, Hafsah A. Sheikh, Sebastian Dowhanik, and Said Aoude. "Investigating the Effect of Δ9-Tetrahydrocannabinol on Brain-derived Neurotropic Factor Levels in Depressed Male Rats." Undergraduate Research in Natural and Clinical Science and Technology (URNCST) Journal 4, no. 2 (February 10, 2020): 1–5. http://dx.doi.org/10.26685/urncst.173.

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Karkashadze, George A., Leyla S. Namazova-Baranova, Leonid M. Yatsik, Olga B. Gordeeva, Elena A. Vishneva, Kamilla E. Efendieva, Elena V. Kaytukova, et al. "Levels of Neurospecific Peptides, Neurotransmitters and Neuroreceptor Markers in the Serum of Children with Various Sensory Disorders, Mild Cognitive Impairments and Other Neuropathology." Pediatric pharmacology 19, no. 6 (January 12, 2023): 459–78. http://dx.doi.org/10.15690/pf.v19i6.2486.

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Background. The role of recently discovered neurospecific peptides in the pathogenesis of acute and progressive neurologic disorders, their neuroprotective features, and possibilities to use them as markers for the course and prognosis of certain diseases have been actively studied in recent decades. However, neurospecific peptides are almost not studied in chronic residual diseases. In our study we measured the levels of neurospecific peptides and some other markers to achieve understanding of general neurophysiological trends in congenital and acquired chronic non-progressive brain pathology with reference to the selection of relevant groups — study objects. Objective. The aim of the study is to study patterns of neurospecific peptides, neurotransmitters and neuroreceptor markers distribution in the serum of children with various pathogenetic variants of chronic neuropathology. Methods. The study included children from 3 to 16 years old with different pathologies. The sample was divided into groups by pathology type: no sensory and neurological disorders, congenital sensory deficit due to mutation of genes expressed and not expressed in the brain, early acquired sensory deficit of multifactorial nature, congenital mild and severe organic disorders of central nervous system (CNS) in residual stage without baseline sensory deficit, acquired functional CNS disorders without baseline organic defect and sensory deficit. The following laboratory data (neurophysiological components) was studied: nerve growth factor, brain-derived neurotropic factor, neurotrophin-3, neurotrophin-4, neuregulin-1-beta-1, beta-secretase, sirtuin-1, synaptophysin, neuronal nitric oxide synthase, and anti-NR2 glutamate receptor antibodies. The parameters of cognitive activity, sense of vision, sense of smell, and acoustic sense were also evaluated. Results. The study included 274 participants. Neuropeptides and markers have shown a variable degree and range in the group spectrum of differences from normal levels. The most variable in the examined sample was NO-synthase, as well as levels of both neurotrophins, beta-secretase, and glutamate receptor marker. All visual deficits were associated with increased NO-synthase levels (p < 0.001). Neuroplasticity peptides (beta-secretase, neurotrophin-3 and 4) have been activated in all pathological conditions. Nerve growth factor and brain-derived neurotropic factor were specifically activated in mild organic CNS lesions (mild cognitive impairments), while neuregulin — in congenital genetically determined visual deficits. There was no specific activation of neuropeptides and NO-synthase level tended to decrease in cases of severe CNS lesions. Conclusion. The study results suggest that all types of early visual impairment are associated with increased physiological neuronal activity, and non-organic neurological functional disorders — mainly with increased physiological synaptic activity. General neuroplasticity processes were activated in all cases of visual deficits but more specific. However, more specific and well-studied processes were activated in mild organic CNS lesions, and neuroplasticity processes did not activate adequately in severe organic CNS lesions probably due to the limited neuronal and synaptic resources.

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Singh, Arjun, and Satish Rattan. "BDNF rescues aging-associated internal anal sphincter dysfunction." American Journal of Physiology-Gastrointestinal and Liver Physiology 321, no. 1 (July 1, 2021): G87—G97. http://dx.doi.org/10.1152/ajpgi.00090.2021.

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These studies demonstrate that brain-derived neurotropic factor (BDNF) rescues the aging-associated internal anal sphincter (IAS) dysfunction, characterized by a decrease in IAS tone, and increase in non-adrenergic noncholinergic relaxation. We determined the effects of BDNF on the basal and GPCR (TXA2 and ANG II)-stimulated IAS tone, and on NANC relaxation, before and after TrkB inhibitor K252a. BDNF may have an important role in the pathophysiology and therapeutic targeting of certain rectoanal motility disorders.

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Lee, Bun-Hee, and Yong-Ku Kim. "Increased Plasma Brain-Derived Neurotropic Factor, Not Nerve Growth Factor-Beta, in Schizophrenia Patients with Better Response to Risperidone Treatment." Neuropsychobiology 59, no. 1 (2009): 51–58. http://dx.doi.org/10.1159/000205518.

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Lesmana, Ronny. "Aerobic Exercise Altered Locomotor Activity and Induced D1 Dopamine Receptor and Brain Derived Neurotropic Factor (BDNF) Expressions." Pakistan Veterinary Journal 39, no. 03 (July 1, 2019): 341–46. http://dx.doi.org/10.29261/pakvetj/2019.070.

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Bruijniks, Sanne J. E., Gerard van Grootheest, Pim Cuijpers, Hilde de Kluiver, Christiaan H. Vinkers, Frenk Peeters, Brenda Penninx, Charlotte E. Teunissen, and Marcus J. H. Huibers. "Working memory moderates the relation between the brain-derived neurotropic factor (BDNF) and psychotherapy outcome for depression." Journal of Psychiatric Research 130 (November 2020): 424–32. http://dx.doi.org/10.1016/j.jpsychires.2020.07.045.

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McKay, Bryon R., Joshua P. Nederveen, Stephen A. Fortino, Tim Snijders, Sophie Joanisse, Dinesh A. Kumbhare, and Gianni Parise. "Brain-derived neurotrophic factor is associated with human muscle satellite cell differentiation in response to muscle-damaging exercise." Applied Physiology, Nutrition, and Metabolism 45, no. 6 (June 2020): 581–90. http://dx.doi.org/10.1139/apnm-2019-0501.

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Muscle satellite cell (SC) regulation is a complex process involving many key signalling molecules. Recently, the neurotrophin brain-derived neurotropic factor (BDNF) has implicated in SC regulation in animals. To date, little is known regarding the role of BDNF in human SC function in vivo. Twenty-nine males (age, 21 ± 0.5 years) participated in the study. Muscle biopsies from the thigh were obtained prior to a bout of 300 maximal eccentric contractions (Pre), and at 6 h, 24 h, 72 h, and 96 h postexercise. BDNF was not detected in any quiescent (Pax7+/MyoD−) SCs across the time-course. BDNF colocalized to 39% ± 5% of proliferating (Pax7+/MyoD+) cells at Pre, which increased to 84% ± 3% by 96 h (P < 0.05). BDNF was only detected in 13% ± 5% of differentiating (Pax7−/MyoD+) cells at Pre, which increased to 67% ± 4% by 96 h (P < 0.05). The number of myogenin+ cells increased 95% from Pre (1.6 ± 0.2 cells/100 myofibres (MF)) at 24 h (3.1 ± 0.3 cells/100 MF) and remained elevated until 96 h (cells/100 MF), P < 0.05. The proportion of BDNF+/myogenin+ cells was 26% ± 0.3% at Pre, peaking at 24 h (49% ± 3%, P < 0.05) and remained elevated at 96 h (P < 0.05). These data are the first to demonstrate an association between SC proliferation and differentiation and BDNF expression in humans in vivo, with BDNF colocalization to SCs increasing during the later stages of proliferation and early differentiation. Novelty BDNF is associated with SC response to muscle injury. BDNF was not detected in nonactivated (quiescent) SCs. BDNF is associated with late proliferation and early differentiation of SCs in vivo in humans.

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Diechmann, Mette D., Evan Campbell, Elaine Coulter, Lorna Paul, Ulrik Dalgas, and Lars G. Hvid. "Effects of Exercise Training on Neurotrophic Factors and Subsequent Neuroprotection in Persons with Multiple Sclerosis—A Systematic Review and Meta-Analysis." Brain Sciences 11, no. 11 (November 12, 2021): 1499. http://dx.doi.org/10.3390/brainsci11111499.

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Background: Evidence indicates that exercise holds the potential to counteract neurodegeneration experienced by persons with multiple sclerosis (pwMS), which is in part believed to be mediated through increases in neurotrophic factors. There is a need to summarize the existing evidence on exercise-induced effects on neurotrophic factors alongside neuroprotection in pwMS. Aim: To (1) systematically review the evidence on acute (one session) and/or chronic (several sessions) exercise-induced changes in neurotrophic factors in pwMS and (2) investigate the potential translational link between exercise-induced changes in neurotrophic factors and neuroprotection. Methods: Five databases (Medline, Scopus, Web of Science, Embase, Sport Discus) were searched for randomized controlled trials (RCT) examining the effects of exercise (all modalities included) on neurotrophic factors as well as measures of neuroprotection if reported. The quality of the study designs and the exercise interventions were assessed by use of the validated tool TESTEX. Results: From N = 337 identified studies, N = 14 RCTs were included. While only N = 2 of the identified studies reported on the acute changes in neurotrophic factors, all N = 14 RCTs reported on the chronic effects, with N = 9 studies revealing between-group differences in favor of exercise. This was most prominent for brain-derived neurotrophic factor (BDNF), with between-group differences in favor of exercise being observed in N = 6 out of N = 12 studies. Meta-analyses were applicable for three out of 10 different identified neurotrophic factors and revealed that exercise can improve the chronic levels of BDNF (delta changes; N = 9, ES = 0.78 (0.27; 1.28), p = 0.003, heterogeneity between studies) and potentially also ciliary neurotrophic factor (CNTF) (N = 3, ES = 0.24 (−0.07; 0.54), p = 0.13, no heterogeneity between studies) but not nerve growth factor (NGF) (N = 4, ES = 0.28 (−0.55; 1.11), p = 0.51, heterogeneity between studies). Indicators of neuroprotection (e.g., with direct measures of brain structure assessed by MRI) were assessed in N = 3 of the identified studies only, with N = 2 partly supporting and thus indicating a potential translational link between increases in neurotrophic factors and neuroprotection. Conclusion: The present study reveals that exercise can elicit improvements in chronic levels of BDNF in pwMS, whereas the effects of exercise on chronic levels of other neurotrophic factors and on acute levels of neurotrophic factors in general, along with a potential translational link (i.e., with exercise-induced improvements in neurotropic factors being associated with or even mediating neuroprotection), are sparse and inconclusive. There is a need for more high-quality studies that assess neurotrophic factors (applying comparable methods of blood handling and analysis) concomitantly with neuroprotective outcome measures. Review Registration: PROSPERO (ID: CRD42020177353).

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Brown, Donnamay T., James C. Vickers, Kimberley E. Stuart, Katerina Cechova, and David D. Ward. "The BDNF Val66Met Polymorphism Modulates Resilience of Neurological Functioning to Brain Ageing and Dementia: A Narrative Review." Brain Sciences 10, no. 4 (March 25, 2020): 195. http://dx.doi.org/10.3390/brainsci10040195.

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Brain-derived neurotropic factor (BDNF) is an abundant and multi-function neurotrophin in the brain. It is released following neuronal activity and is believed to be particularly important in strengthening neural networks. A common variation in the BDNF gene, a valine to methionine substitution at codon 66 (Val66Met), has been linked to differential expression of BDNF associated with experience-dependent plasticity. The Met allele has been associated with reduced production of BDNF following neuronal stimulation, which suggests a potential role of this variation with respect to how the nervous system may respond to challenges, such as brain ageing and related neurodegenerative conditions (e.g., dementia and Alzheimer’s disease). The current review examines the potential of the BDNF Val66Met variation to modulate an individual’s susceptibility and trajectory through cognitive changes associated with ageing and dementia. On balance, research to date indicates that the BDNF Met allele at this codon is potentially associated with a detrimental influence on the level of cognitive functioning in older adults and may also impart increased risk of progression to dementia. Furthermore, recent studies also show that this genetic variation may modulate an individual’s response to interventions targeted at building cognitive resilience to conditions that cause dementia.

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Hendriati, Deasy, Elemeida Effendy, Mustafa Mahfud Amin, Vita Camellia, and Muhammad Surya Husada. "Brain-Derived Neurotropic Factor Serum Level and Severity Symptom of Bataknese Male Patients with Schizophrenia in North Sumatera, Indonesia." Open Access Macedonian Journal of Medical Sciences 7, no. 12 (July 6, 2019): 1957–61. http://dx.doi.org/10.3889/oamjms.2019.550.

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BACKGROUND: Schizophrenia is a severe mental disorder that is multi-causative and multi-factor, generally affecting about 1% of the population. The elevation level of brain-derived neurotrophic factor (BDNF) offers several protections from other neurodegenerative processes that occur in schizophrenia since this deficit of neurotrophic factors can contribute to changes in brain structure and function that underlie the schizophrenia psychopathology.AIM: To analyse the correlation between BDNF serum levels and symptom severity by using the Positive and Negative Syndrome Scale (PANSS) instrument in Bataknese male patients with schizophreniaMETHODS: This study was a correlative analytical study with a cross-sectional approach using the Positive and Negative Syndrome Scale (PANSS) instrument to assess symptom severity with 60 subjects of Bataknese male patients with chronic schizophrenia. Moreover, this research was conducted at the Psychiatric Hospital of Prof. Dr M. Ildrem Medan, Indonesia. BDNF serum was analysed with the Quantitative sandwich enzyme immunoassay technique by via Quantikine ELISA Human CXCL8/IL-8 HS. Also, the data analysis was performed through Spearman's correlative bivariate analytics using SPSS software.RESULTS: A negative correlation between the BDNF serum level and the negative scale PANSS score in men with schizophrenia (r = -0.820, p < 0.001) was found. Moreover, there is a negative correlation between BDNF serum levels and PANSS total scores in men with schizophrenia (r = -0.648, p < 0.001)CONCLUSION: BDNF serum level in Bataknese male patients with schizophrenia has a relationship that affects the severity of symptoms in schizophrenic patients, especially for negative symptoms.

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Choi, Ga-Young, Hyun-Bum Kim, Eun-Sang Hwang, Seok Lee, Min-Ji Kim, Ji-Young Choi, Sung-Ok Lee, Sang-Seong Kim, and Ji-Ho Park. "Curcumin Alters Neural Plasticity and Viability of Intact Hippocampal Circuits and Attenuates Behavioral Despair and COX-2 Expression in Chronically Stressed Rats." Mediators of Inflammation 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/6280925.

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Curcumin is a major diarylheptanoid component ofCurcuma longawith traditional usage for anxiety and depression. It has been known for the anti-inflammatory, antistress, and neurotropic effects. Here we examined curcumin effect in neural plasticity and cell viability. 60-channel multielectrode array was applied on organotypic hippocampal slice cultures (OHSCs) to monitor the effect of 10 μM curcumin in long-term depression (LTD) through low-frequency stimulation (LFS) to the Schaffer collaterals and commissural pathways. Cell viability was assayed by propidium iodide uptake test in OHSCs. In addition, the influence of oral curcumin administration on rat behavior was assessed with the forced swim test (FST). Finally, protein expression levels of brain-derived neurotrophic factor (BDNF) and cyclooxygenase-2 (COX-2) were measured by Western blot in chronically stressed rats. Our results demonstrated that 10 μM curcumin attenuated LTD and reduced cell death. It also recovered the behavior immobility of FST, rescued the attenuated BDNF expression, and inhibited the enhancement of COX-2 expression in stressed animals. These findings indicate that curcumin can enhance postsynaptic electrical reactivity and cell viability in intact neural circuits with antidepressant-like effects, possibly through the upregulation of BDNF and reduction of inflammatory factors in the brain.

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