Mild traumatic brain injury and delayed alteration of memory processing

• Published in: Frontiers in neuroscience Vol. 9; p. 369
• Main Author: Foster, Philip P
• Format: Journal Article
• Language: English
• Published: Switzerland Frontiers Research Foundation 14-10-2015; Frontiers Media S.A
• Subjects: Aging; Amyloid; BDNF; Brain-derived neurotrophic factor; Cognitive ability; Default Mode Network; Epigenetics; fMRI; Fractals; Hippocampal plasticity; Hippocampus; Medical imaging; Memory; Nanotechnology; Neural networks; Neuroimaging; Neurological complications; Neuroscience; Phenotypes; Senile plaques; Single nucleotide polymorphism; Skeletal muscle; Sleep; Synaptic plasticity; Traumatic brain injury; United States > US; fMRI; hippocampus; BDNF; salience network; single nucleotide polymorphism; MTBI; default mode network; relational memory
• ISSN: 1662-4548; 1662-453X; 1662-453X
• DOI: 10.3389/fnins.2015.00369

Disconnection of brain networks (Sharp et al., 2014) may be irreversible and further induce neurological or cognitive impairment such as relational memory described in Monti's paper. Because irreversible post-TBI damage may occur and determination of longitudinal changes in connectomics is problematic (Goh et al., 2015), innovative diagnostic tools such as connectomic imaging, specifically for inter-regional connectivity (Irimia et al., 2014), are desired. Wrong assignments and characteristics specific to the micro-scale such as biophysical, biochemical and functional interactions of DNA (gene sequences), RNA or metabolites may be completely dysregulated and, therefore, biomarkers may be produced by this abnormal functioning and further serve for diagnotics purposes. Genes modifying the hippocampal phenotype (e.g., BDNF), possibly upregulated by epigenetic factors such as skeletal muscle exercise, are known for synaptic molding and hippocampal plasticity and recent studies have shown that the Val66Met BDNF polymorphism has been involved in greater resilience and recovery potential of higher-order executive functions to TBI than Val66Val BDNF carriers (Barbey et al., 2014). A threshold is attained when the concurrent addition or succession of DAI, amyloid-β plaques and dysfunction of large-scale neural networks lead to clinical symptoms of mild cognitive impairment.