Modelling organelle transport after traumatic axonal injury

• Published in: Computer methods in biomechanics and biomedical engineering Vol. 18; no. 6; pp. 583 - 591
• Main Authors: Kuznetsov, I.A., Kuznetsov, A.V.
• Format: Journal Article
• Language: English
• Published: England Taylor & Francis 26.04.2015
• Subjects: Animals; Axons - metabolism; Axons - physiology; Brain Injuries - physiopathology; Computer Simulation; Diffusion; fast axonal transport; Humans; intracellular organelles; microtubules; Microtubules - metabolism; Models, Neurological; molecular motors; neurons; Organelles - metabolism; traumatic brain injury; fast axonal transport; traumatic brain injury; microtubules; intracellular organelles; molecular motors; neurons
• DOI: 10.1080/10255842.2013.820721
• ISSN: 1025-5842; 1476-8259

This paper is motivated by recent experimental research (Tang-Schomer et al. 2012) on the formation of periodic varicosities in axons after traumatic brain injury (TBI). TBI leads to the formation of undulated distortions in the axons due to their dynamic deformation. These distortions result in the breakage of some microtubules (MTs) near the peaks of undulations. The breakage is followed by catastrophic MT depolymerisation around the broken ends. Although after relaxation axons regain their straight geometry, the structure of the axon after TBI is characterised by the presence of periodic regions where the density of MTs has been decreased due to depolymerisation. We modelled organelle transport in an axon segment with such a damaged MT structure and investigated how this structure affects the distributions of organelle concentrations and fluxes. The modelling results suggest that organelles accumulate at the boundaries of the region where the density of MTs has been decreased by depolymerisation. According to the model, the presence of such damaged regions decreases the organelle flux by only about 12%. This provides evidence that axon degradation after TBI may be caused by organelle accumulation rather than by starvation due to insufficient organelle flux.