Skip to main content
Article thumbnail
Location of Repository

Role of physical and mental training in brain network configuration

By Philip P. Foster

Abstract

Continuous remodeling of proteins of excitatory neurons is fine-tuning the scaling and strength of excitatory synapses up or down via regulation of intra-cellular metabolic and regulatory networks of the genome-transcriptome-proteome interface. Alzheimer's disease is a model of energy cost-driven small-world network disorder as the network global efficiency is impaired by the deposition of an informed agent, the amyloid-β, selectively targeting high-degree nodes. In schizophrenia, the interconnectivity and density of rich-club networks are significantly reduced. Training-induced homeostatic synaptogenesis-enhancement produces a reconfiguration of brain networks into greater small-worldness. Creation of synaptic connections in a macro-network, and, at the intra-cellular scale, micro-networks regulate the physiological mechanisms for the preferential attachment of synapses. The strongest molecular relationship of exercise and functional connectivity was identified for brain-derived neurotrophic factor (BDNF). The allele variant, rs7294919, also shows a powerful relationship with the hippocampal volume. How the brain achieves this unique quest of reconfiguration remains a puzzle. What are the underlying mechanisms of synaptogenesis promoting communications brain ↔ muscle and brain ↔ brain in such trainings? What is the respective role of independent mental, physical or combined-mental-physical trainings? Physical practice seems to be playing an instrumental role in the cognitive enhancement (brain ↔ muscle com.). However, mental training, meditation or virtual reality (films, games) require only minimal motor activity and cardio-respiratory stimulation. Therefore, other potential paths (brain ↔ brain com.) molding brain networks are nonetheless essential. Patients with motor neuron disease/injury (e.g. amyotrophic lateral sclerosis, traumatism) also achieve successful cognitive enhancement albeit they may only elicit mental practic

Topics: Amyloid beta-Peptides, CA1 Region, Hippocampal, Dentate Gyrus, Depression, Entorhinal Cortex, GABA Antagonists, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571
Publisher: Frontiers Media S.A.
Year: 2015
DOI identifier: 10.3389/fnagi.2015.00117
OAI identifier: oai:doaj.org/article:288c6e0c320b4f7eb3966bc64eb41467
Journal:
Download PDF:
Sorry, we are unable to provide the full text but you may find it at the following location(s):
  • https://doaj.org/toc/1663-4365 (external link)
  • http://journal.frontiersin.org... (external link)
  • https://doaj.org/article/288c6... (external link)
  • Suggested articles


    To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.