We describe the evolution of axonal injury following the induction of neural damage by electrical stimulation. The sciatic nerves of cats were stimulated continuously for 8 h with charge-balanced waveforms at high intensities, 50 Hz and 2100-4500 microA, using circumneural helical electrodes. Computer-assisted morphometric and ultrastructural studies indicate that many of the damaged fibers had not regenerated by 125 days after stimulation. Functional deficits were not observed in any of the animals, and most of the fibers appeared to be histologically normal at 125 days after stimulation. These findings indicate that there is relatively little late-onset injury associated with the stimulation. However, the slow, and possibly incomplete, recovery of the damaged axons emphasizes the importance of using stimulus protocols with adequate margins of safety.
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http://dx.doi.org/10.1002/(sici)1097-4598(199910)22:10<1393::aid-mus9>3.0.co;2-e | 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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