This study aims to clarify the relation between axonal deformation and the onset of axonal injury. Firstly, to examine the influence of strain rate on the threshold for axonal injury, cultured neurons were subjected to 12 types of stretching (strains were 0.10, 0.15, and 0.20 and strain rates were 10, 30, 50, and 70 s). The formation of axonal swellings and bulbs increased significantly at strain rates of 50 and 30 s with strains of 0.15 and 0.20, respectively, even though those formations did not depend on strain rates in cultures exposed to a strain of 0.10. Then, to examine the influence of the strain along an axon on axonal injury, swellings were measured at every axonal angle in the stretching direction. The axons that were parallel to stretching direction were injured the most. Finally, we proposed an experimental model that subjected an axon to more accurate strain. This model observed the process of axonal injury formation by detecting the same neuron before and after stretching. These results suggest that the strain-rate dependency of axonal tolerance is induced by a higher magnitude of loading strain and an experiment focusing on axonal strain is required for obtaining more detailed injury criteria for an axon.
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http://dx.doi.org/10.4271/2017-22-0003 | DOI Listing |
Ann Neurol
January 2025
Department of Neurology, University of Massachusetts Chan Medical School, Worcester, MA.
Objective: Approximately 20% of familial cases of amyotrophic lateral sclerosis (ALS) are caused by mutations in the gene encoding superoxide dismutase 1 (SOD1). Epidemiological data have identified traumatic brain injury (TBI) as an exogenous risk factor for ALS; however, the mechanisms by which TBI may worsen SOD1 ALS remain largely undefined.
Methods: We sought to determine whether repetitive TBI (rTBI) accelerates disease onset and progression in the transgenic SOD1 mouse ALS model, and whether loss of the primary regulator of axonal degeneration sterile alpha and TIR motif containing 1 (Sarm1) mitigates the histological and behavioral pathophysiology.
ACS Chem Neurosci
January 2025
Department of Neurology, Multi-Omics Research Center for Brain Disorders,The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.
Brachial plexus root avulsion (BPRA) is often caused by road collisions, leading to total loss of motor function in the upper limb. At present, effective treatment options remain limited. Edaravone (EDA), a substance that eliminates free radicals, exhibits numerous biological properties, including neuroprotective, antioxidant and anti-inflammatory effects.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Ophthalmology, Keck School of Medicine, USC Roski Eye Institute, University of Southern California, Los Angeles, California, United States of America.
Failure of central nervous system (CNS) axons to regenerate after injury results in permanent disability. Several molecular neuro-protective and neuro-regenerative strategies have been proposed as potential treatments but do not provide the directional cues needed to direct target-specific axon regeneration. Here, we demonstrate that applying an external guidance cue in the form of electric field stimulation to adult rats after optic nerve crush injury was effective at directing long-distance, target-specific retinal ganglion cell (RGC) axon regeneration to native targets in the diencephalon.
View Article and Find Full Text PDFBackground: Neurofilament Light Chain (NfL) is a blood biomarker of axonal injury and neurodegeneration that can be used in a variety of neurological disorders. Despite the potential clinical use of plasma NfL across multiple neurological disorders, there is increasing evidence that underlying comorbidities such as renal impairment associated with chronic kidney disease (CKD) and cardiovascular diseases can increase NfL concentrations. The objective of this study was to determine the relationship between plasma NfL concentrations and renal function (CKD staging) in individuals without known neurological conditions.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Southern California, Los Angeles, CA, USA.
Background: Plasma neurofilament light (NfL) and glial fibrillary acidic protein (GFAP) are markers of axonal and astroglial injury, respectively. Both markers have been proposed as predictive biomarkers of cerebral small vessel disease, with elevated levels indicating higher burden of white matter hyperintensities, lacunar infarcts and cerebral microbleeds. However, to date, no study has examined whether NfL and GFAP levels are associated with dynamic markers of small vessel damage such as cerebrovascular reactivity (CVR)-the ability of cerebral blood vessels to regulate cerebral blood flow (CBF) in response to vasodilatory or vasoconstrictive stimuli.
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