CONTACT US: Contact info
|
Citation |
Horstemeyer MF, Berthelson PR, Moore J, Persons AK, Dobbins A, Prabhu RK. Ann. Biomed. Eng. 2019; ePub(ePub): ePub. |
|
Affiliation |
Department of Agricultural and Biological Engineering, Mississippi State University, 130 Creelman St., Starkville, MS, 39762, USA. |
|
Copyright |
(Copyright © 2019, Holtzbrinck Springer Nature Publishing Group) |
|
DOI |
|
PMID |
31372858 |
|
Abstract |
A mechanics-based brain damage framework is used to model the abnormal accumulation of hyperphosphorylated p-tau associated with chronic traumatic encephalopathy within the brains of deceased National Football League (NFL) players studied at Boston University and to provide a framework for understanding the damage mechanisms. p-tau damage is formulated as the multiplicative decomposition of three independently evolving damage internal state variables (ISVs): nucleation related to number density, growth related to the average area, and coalescence related to the nearest neighbor distance. The ISVs evolve under different rates for three well known mechanical boundary conditions, which in themselves introduce three different rates making a total of nine scenarios, that we postulate are related to brain damage progression: (1) monotonic overloads, (2) cyclic fatigue which corresponds to repetitive impacts, and (3) creep which is correlated to damage accumulation over time. Different NFL player positions are described to capture the different types of damage progression. Skill position players, such as quarterbacks, are expected to exhibit a greater p-tau protein accumulation during low cycle fatigue (higher amplitude impacts with a lesser number), and linemen who exhibit a greater p-tau protein accumulation during high cycle fatigue (lower amplitude impacts with a greater number of impacts). This mechanics-based damage framework presents a foundation for developing a multiscale model for traumatic brain injury that combines mechanics with biology. Language: en |
|
Keywords |
Creep; Damage coalescence; Damage growth; Damage nucleation; Fatigue; Internal state variable theory; Overloads; Traumatic brain injury |