Abstract

The perineuronal net (PNN) region of the brain’s extracellular matrix (ECM) surrounds the neural networks within the brain tissue. The PNN is a protective net-like structure regulating neuronal activity such as neurotransmission, charge balance, and action potential generation. Shock-induced damage of this essential component may lead to neuronal cell death and neurodegenerations. The shock generated during a vehicle accident, fall, or improvised device explosion may produce sufficient energy to damage the structure of the PNN. The goal is to investigate the mechanics of the PNN in reaction to shock loading and to understand the mechanical properties of different PNN components such as glycan, GAG, and protein. In this study, we evaluated the mechanical strength of PNN molecules and the interfacial strength between the PNN components. Afterward, we assessed the PNN molecules’ damage efficiency under various conditions such as shock speed, preexisting bubble, and boundary conditions. The secondary structure altercation of the protein molecules of the PNN was analyzed to evaluate damage intensity under varying shock speeds. At a higher shock speed, damage intensity is more elevated, and hyaluronan (glycan molecule) is most likely to break at the rigid junction. The primary structure of the protein molecules is least likely to fail. Instead, the molecules’ secondary bonds will be altered. Our study suggests that the number of hydrogen bonds during the shock wave propagation is reduced, which leads to the change in protein conformations and damage within the PNN structure. As such, we found a direct connection between shock wave intensity and PNN damage.

Highlights

  • Concussion, subconcussions, and exposure to an explosive blast’s shock waves can cause mild traumatic brain injury [1]

  • The core protein (CP) is a very long protein coil chain that forms a secondary structure known as alpha-helix and beta-sheet

  • The non-reactive CHARMM36 force field is advantageous over the reactive because it is widely used for biomolecules, and simulation time is faster than the ReaxFF reactive force field

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Summary

Introduction

Concussion, subconcussions, and exposure to an explosive blast’s shock waves can cause mild traumatic brain injury (mTBI) [1]. A typical blast-induced shock wave profile exhibits a sudden increase in pressure, often called overpressure, followed by a low magnitude with a longer duration negative pressure tail [2]. A typical blast can generate an initial overpressure of over 27 GPa [3]. The shock wave from the blast can travel at a speed several times higher than the sound speed of the medium; for example, in an underwater explosion the shock wave can travel several thousand meters per second [4,5]. The long-range negative pressure tail causes damage to the extracellular matrix (ECM) and neuronal cells by forming a micro cavitation [2,6] and causing mechanical fracture of different biomolecules [6–9]. The overpressure generates a compressive load, which may cause shear fracture of biomolecules

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