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Research Paper|Volume 9, Issue 2|pp 393—407

Computerized cognitive training and brain derived neurotrophic factor during bed rest: mechanisms to protect individual during acute stress

Angelina Passaro1,11, Cecilia Soavi1,11, Uros Marusic2, Enrico Rejc3, Juana M. Sanz1, Mario L. Morieri1, Edoardo Dalla Nora1, Voyko Kavcic4,5, Marco V. Narici6, Carlo Reggiani7, Gianni Biolo8, Giovanni Zuliani1, Stefano Lazzer9,10, Rado Pišot2
  • 1Medical Science Department, University of Ferrara, Ferrara 44121, Italy
  • 2Science and Research Centre, University of Primorska, Koper 6000, Slovenia
  • 3Kentucky Spinal Cord Injury Research Center, University of Louisville, Louisville, KY 40202, USA
  • 4Institute of Gerontology, Wayne State University, Detroit, MI 48202, USA
  • 5Biomedical Research and Innovative Society, Ljubljana 1000, Slovenia
  • 6School of Graduate Entry Medicine and Health, University of Nottingham, Derby DE22 3NE, UK
  • 7Department of Biomedical Sciences, University of Padua, Padua 35131 Italy
  • 8Department of Medical, Surgical and Health Sciences, Division of Internal Medicine, University of Trieste, Trieste 34149, Italy
  • 9Department of Medical and Biological Sciences, University of Udine, Udine 33100, Italy
  • 10School of Sport Sciences, University of Udine, Udine 33100, Italy
  • 11Co-first authors

* * Equal contribution

Received: October 15, 2016Accepted: January 25, 2017Published: February 3, 2017

Copyright: © 2017 Passaro et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Acute stress, as bed rest, was shown to increase plasma level of the neurotrophin brain-derived neurotrophic factor (BDNF) in older, but not in young adults. This increase might represent a protective mechanism towards acute insults in aging subjects. Since computerized cognitive training (CCT) is known to protect brain, herein we evaluated the effect of CCT during bed rest on BDNF, muscle mass, neuromuscular function and metabolic parameters. The subjects that underwent CCT did not show an increase of BDNF after bed rest, and showed an anti-insular modification pattern in metabolism. Neuromuscular function parameters, already shown to beneficiate from CCT, negatively correlated with BDNF in research participants undergoing CCT, while positively correlated in the control group. In conclusion, BDNF increase can be interpreted as a standardized protective mechanism taking place whenever an insult occurs; it gives low, but consistent preservation of neuromuscular function. CCT, acting as an external protective mechanism, seems to modify this standardized response, avoiding BDNF increase or possibly modifying its time course. Our results suggest the possibility of differential neuroprotective mechanisms among ill and healthy individuals, and the importance of timing in determining the effects of protective mechanisms.