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
- 1 Medical Science Department, University of Ferrara, Ferrara 44121, Italy
- 2 Science and Research Centre, University of Primorska, Koper 6000, Slovenia
- 3 Kentucky Spinal Cord Injury Research Center, University of Louisville, Louisville, KY 40202, USA
- 4 Institute of Gerontology, Wayne State University, Detroit, MI 48202, USA
- 5 Biomedical Research and Innovative Society, Ljubljana 1000, Slovenia
- 6 School of Graduate Entry Medicine and Health, University of Nottingham, Derby DE22 3NE, UK
- 7 Department of Biomedical Sciences, University of Padua, Padua 35131 Italy
- 8 Department of Medical, Surgical and Health Sciences, Division of Internal Medicine, University of Trieste, Trieste 34149, Italy
- 9 Department of Medical and Biological Sciences, University of Udine, Udine 33100, Italy
- 10 School of Sport Sciences, University of Udine, Udine 33100, Italy
- 11 Co-first authors
Received: October 15, 2016 Accepted: January 25, 2017 Published: February 3, 2017
https://doi.org/10.18632/aging.101166How to Cite
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.