The spinal cord contains multiple fiber tracts necessary for locomotion. However, as a part of the central nervous system, they are extremely limited in regenerating after injury. Many of these key fiber tracts originate from deep brain stem nuclei that are difficult to access. Here we detail a new methodology that achieves functional regeneration in mice after a complete spinal cord crush, describing the crushing procedure itself, intracortical treatment application, and a set of appropriate validation steps. The regeneration is achieved by the one-time transduction of neurons in the motor cortex with a viral vector expressing the designer cytokine hIL-6. This potent stimulator of the JAK/STAT3 pathway and regeneration is transported in axons and then transneuronally delivered to critical deep brain stem nuclei via collateral axon terminals, resulting in previously paralyzed mice walking again after 3-6 weeks. With no previously known strategy accomplishing this degree of recovery, this model is well suited to studying the functional impact of compounds/treatments currently only known to promote anatomical regeneration.
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http://dx.doi.org/10.1007/978-1-0716-3012-9_6 | DOI Listing |
BMC Neurol
January 2025
Department of Neurology, The First Affiliated Hospital of Zhengzhou University, 1 East Jianshe Road, Zhengzhou, China.
Background: Awareness of the characteristics of glial fibrillary acidic protein autoantibody (GFAP-IgG) associated myelitis facilitates early diagnosis and treatment. We explored features in GFAP-IgG myelitis and compared them with those in myelitis associated with aquaporin-4 IgG (AQP4-IgG) and myelin oligodendrocyte glycoprotein IgG (MOG-IgG).
Methods: We retrospectively reviewed data from patients with GFAP-IgG myelitis at the First Affiliated Hospital of Zhengzhou University and Henan Children's Hospital from May 2018 to May 2023.
BMC Neurosci
January 2025
Laboratory of Veterinary Internal Medicine, Department of Clinical Veterinary Science, College of Veterinary Medicine, Seoul National University, Seoul, 08826, Republic of Korea.
Microglia/macrophages participate in the development of and recovery from experimental autoimmune encephalomyelitis (EAE), and the macrophage M1 (pro-inflammatory)/M2 (anti-inflammatory) phase transition is involved in EAE disease progression. We evaluated the efficacy of crisdesalazine (a novel microsomal prostaglandin E2 synthase-1 inhibitor) in an EAE model, including its immune-regulating potency in lipopolysaccharide-stimulated macrophages, and its neuroprotective effects in a macrophage-neuronal co-culture system. Crisdesalazine significantly alleviated clinical symptoms, inhibited inflammatory cell infiltration and demyelination in the spinal cord, and altered the phase of microglial/macrophage and regulatory T cells.
View Article and Find Full Text PDFSci China Life Sci
December 2024
Clinical and Translational Research Center of Shanghai First Maternity & Infant Hospital, Frontier Science Center for Stem Cells, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China.
Inflammation is a driving force of hematopoietic stem cells (HSCs) aging, causing irreversible exhaustion of functional HSCs. However, the underlying mechanism of HSCs erosion by inflammatory insult remains poorly understood. Here, we find that transient LPS exposure primes aged HSCs to undergo accelerated differentiation at the expense of self-renewal, leading to depletion of HSCs.
View Article and Find Full Text PDFSpinal Cord
January 2025
McKnight Brain Institute, University of Florida, Gainesville, FL, USA.
Study Design: Experimental Animal Study.
Objective: To continue validating an antibody which targets an epitope of neurofilament light chain (NF-L) only available during neurodegeneration and to utilize the antibody to describe the pattern of axonal degeneration 10 days post-unilateral C4 contusion in the rat.
Setting: University of Florida laboratory in Gainesville, USA.
CNS Neurosci Ther
January 2025
Dongguan Key Laboratory of Stem Cell and Regenerative Tissue Engineering, the First Dongguan Affiliated Hospital, School of Basic Medical Sciences, Guangdong Medical University, Dongguan, China.
Aims: Neuron death is caused primarily by apoptosis after spinal cord injury (SCI). Autophagy, as a cellular response, can maintain cellular homeostasis to reduce apoptosis. We aimed to investigate the effect and the mechanism of vimentin knockdown on autophagy and neural recovery after SCI.
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