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Graphene oxide scaffolds promote functional improvements mediated by scaffold-invading axons in thoracic transected rats.

Bioact Mater

May 2025

Instituto de Ciencia de Materiales de Madrid (ICMM), Consejo Superior de Investigaciones Científicas (CSIC), Calle Sor Juana Inés de la Cruz 3, 28049, Madrid, Spain.

Millions of patients and their caretakers live and deal with the devastating consequences of spinal cord injury (SCI) worldwide. Despite outstanding advances in the field to both understand and tackle these pathologies, a cure for SCI patients, with their peculiar characteristics, is still a mirage. One of the most promising therapeutic strategies to date for these patients involves the use of epidural electrical stimulation.

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Effect of Low-Dose Methylprednisolone in Promoting Neurological Function Recovery after Spinal Cord Injury: Clinical and Animal Studies.

Spine (Phila Pa 1976)

January 2025

Department of Orthopedics, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People's Republic of China.

Study Design: Subgroup analysis of a retrospective clinical and animal trial [Study of different doses of methylprednisolone on functional recovery of spinal cord injury].

Objective: The aimed to investigate the efficacy of low-dose methylprednisolone regimens in promoting neural repair after SCI.

Summary Of Background Data: Spinal cord injury (SCI) can result in sensory, motor, and autonomic nerve dysfunction, often leading to disability or death.

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Axonal fusion represents an efficient way to recover function after nerve injury. However, how axonal fusion is induced and regulated remains largely unknown. We discover that ferroptosis signaling can promote axonal fusion and functional recovery in C.

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The transcriptional response of cortical neurons to concussion reveals divergent fates after injury.

Nat Commun

January 2025

Unit on the Development of Neurodegeneration, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA.

Traumatic brain injury (TBI) is a risk factor for neurodegeneration, however little is known about how this kind of injury alters neuron subtypes. In this study, we follow neuronal populations over time after a single mild TBI (mTBI) to assess long ranging consequences of injury at the level of single, transcriptionally defined neuronal classes. We find that the stress-responsive Activating Transcription Factor 3 (ATF3) defines a population of cortical neurons after mTBI.

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Axons in the mammalian brain show significant diversity in myelination motifs, displaying spatial heterogeneity in sheathing along individual axons and across brain regions. However, its impact on neural signaling and susceptibility to injury remains poorly understood. To address this, we leveraged cable theory and developed model axons replicating the myelin sheath distributions observed experimentally in different regions of the mouse central nervous system.

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