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Role of physical and mental training in brain network configuration

By Philip P. Foster


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
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