Faculty Opinions recommendation of Brain-Derived Neurotrophic Factor Val66Met Human Polymorphism Impairs the Beneficial Exercise-Induced Neurobiological Changes in Mice.

Author(s):  
Henriette van Praag
2016 ◽  
Vol 41 (13) ◽  
pp. 3070-3079 ◽  
Author(s):  
Alessandro Ieraci ◽  
Alessandro I Madaio ◽  
Alessandra Mallei ◽  
Francis S Lee ◽  
Maurizio Popoli

2021 ◽  
Author(s):  
Sarah Ahmad ◽  
Rodney Hansen ◽  
Matthew Schmolesky

AbstractResearch suggests strong inter-relationships between physical exercise, levels of brain-derived neurotrophic factor (BDNF), levels of estrogen, and the menstrual cycle, and yet no single study has examined these factors collectively in humans. The current study assessed the effect of an acute bout of vigorous aerobic exercise (20 minutes of stationary cycling at 80% of heart rate reserve) on serum BDNF and estradiol in healthy, eumenorrheic women, ages 18-28. In addition, this study determined whether basal BDNF or the exercise-induced increase in BDNF varies throughout the menstrual cycle. Thirty-four subjects were assigned to an experimental (n = 27) or control condition (n = 7). Exercise transiently increased both estradiol (51.2%) and BDNF (23.6%), and basal levels of BDNF and estradiol predicted the magnitude of the exercise-induced increases. Basal BDNF did not vary significantly throughout the menstrual cycle. Exercise-induced changes in BDNF did not correlate with menstrual cycle day or basal estradiol. Basal estradiol and basal BDNF showed a marginally significant positive correlation. Taken together, these results indicate that brief, vigorous aerobic exercise is sufficient to elevate both BDNF and estradiol in healthy women and that the menstrual cycle dramatically influences the magnitude of exercise-induced changes in estradiol, but not BDNF


2009 ◽  
Vol 94 (12) ◽  
pp. 1153-1160 ◽  
Author(s):  
Bente K. Pedersen ◽  
Maria Pedersen ◽  
Karen S. Krabbe ◽  
Helle Bruunsgaard ◽  
Vance B. Matthews ◽  
...  

1998 ◽  
Vol 61 (1-2) ◽  
pp. 147-153 ◽  
Author(s):  
Heather S. Oliff ◽  
Nicole C. Berchtold ◽  
Paul Isackson ◽  
Carl W. Cotman

2010 ◽  
Vol 479 (2) ◽  
pp. 161-165 ◽  
Author(s):  
Joshua F. Yarrow ◽  
Lesley J. White ◽  
Sean C. McCoy ◽  
Stephen E. Borst

2016 ◽  
Vol 120 (1) ◽  
pp. 70-87 ◽  
Author(s):  
Angelo Russo ◽  
Livia Buratta ◽  
Roberto Pippi ◽  
Cristina Aiello ◽  
Claudia Ranucci ◽  
...  

Exercise-mediated, brain-derived neurotrophic factor induction benefits health and cognitive functions. The multifaceted interplay between physical activity, urinary brain-derived neurotrophic factor levels and cognitive functioning has been largely neglected in previous literature. In this pilot study, two bouts of training exercise (65% and 70% of heart rate reserve) influenced urinary brain-derived neurotrophic factor levels and cognitive performances in 12 overweight and obese participants. Percent heart rate reserve, expenditure energy, brain-derived neurotrophic factor urinary levels and cognitive performances were measured before and after the exercise. No significant variations in energy expenditure were observed, while differences of heart rate reserve between two groups were maintained. Both bouts of training exercise induced a similar reduction in urinary brain-derived neurotrophic factor levels. Only visuo-spatial working memory capacity at 65% of heart rate reserve showed a significant increase. These findings indicate a consistent effect of training exercise on urinary brain-derived neurotrophic factor levels and cognitive factors in overweight and obese participants.


2008 ◽  
Vol 40 (11) ◽  
pp. 1990-1996 ◽  
Author(s):  
MAAIKE GOEKINT ◽  
ELSA HEYMAN ◽  
BART ROELANDS ◽  
ROSE NJEMINI ◽  
IVAN BAUTMANS ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Brooke H. Van Kummer ◽  
Randy W. Cohen

Moderate aerobic exercise has been shown to enhance motor skills and protect the nervous system from neurodegenerative diseases, like ataxia. Our lab uses thespasticHan Wistar rat as a model of ataxia. Mutant rats develop forelimb tremor and hind limb rigidity and have a decreased lifespan. Our lab has shown that exercise reduced Purkinje cell degeneration and delayed motor dysfunction, significantly increasing lifespan. Our study investigated how moderate exercise may mediate neuroprotection by analyzing brain-derived neurotrophic factor (BDNF) and its receptor TrkB. To link BDNF to exercise-induced neuroprotection, mutant and normal rats were infused with the TrkB antagonist K252a or vehicle into the third ventricle. During infusion, rats were subjected to moderate exercise regimens on a treadmill. Exercised mutants receiving K252a exhibited a 21.4% loss in Purkinje cells compared to their controls. Cerebellar TrkB expression was evaluated using non-drug-treated mutants subjected to various treadmill running regimens. Running animals expressed three times more TrkB than sedentary animals. BDNF was quantified via Sandwich ELISA, and cerebellar expression was found to be 26.6% greater in mutant rats on 7-day treadmill exercise regimen compared to 30 days of treadmill exercise. These results suggest that BDNF is involved in mediating exercise-induced neuroprotection.


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