VA San Diego Healthcare System, San Diego, CA, USA; Dept. of Neurosciences, University of California - San Diego, La Jolla, CA, USA. Electronic address:
Published: September 2024
AI Article Synopsis
Article Abstract
Neuroscience dogma avers that astrocytic "scars" inhibit axonal regeneration after spinal cord injury (SCI). A recent report suggested however that astrocytes form "borders" around lesions that are permissive rather than inhibitory to axonal growth. We now provide further evidence supporting a facilitatory role of astrocytes in axonal regeneration after SCI. First, even 6months after SCI, injured axons are retained within regions of densely reactive astrocytes, in direct contact with astrocyte processes without being repelled. Second, 6 month-delayed implants of neural stem cells extend axons into reactive astrocyte borders surrounding lesions, densely contacting astrocyte surfaces. Third, bioengineered hydrogels implanted into sites of SCI re-orient reactive astrocytic processes to align along the rostral-to-caudal spinal cord axis resulting in successful regeneration into the lesion/scaffold in close association with astrocytic processes. Fourth, corticospinal axons regenerate into neural progenitor cells implanted six months after injury in close association with host astrocytic processes. Thus, astrocytes do not appear to inhibit axonal regeneration, and the close association of newly growing axons with astrocytic processes suggests a facilitatory role in axonal regeneration.
Central Laboratory of The Lishui Hospital of Wenzhou Medical University, The First Affiliated Hospital of Lishui University, Lishui People's Hospital, Lishui, Zhejiang, China.
Introduction: Spinal cord injury (SCI) is a severe neurological disease characterized by significant motor, sensory, and autonomic dysfunctions. SCI is a major global disability cause, often resulting in long-term neurological impairments due to the impeded regeneration and remyelination of axons. A SCI interferes with communication between the brain and the spinal cord networks that control neurological functions.
Background: Mild traumatic brain injury (mTBI) frequently results in persistent cognitive, emotional, and functional impairments, closely linked to disruptions in the default mode network (DMN). Understanding the mechanisms driving these network abnormalities is critical for advancing diagnostic and therapeutic strategies.
Methods: This study adopted a multimodal approach, combining functional connectivity (FC) analysis, diffusion tensor imaging (DTI), and gene expression profiling to investigate DMN disruptions in mTBI.
With no effective treatments for functional recovery after injury, spinal cord injury (SCI) remains one of the unresolved healthcare challenges. Human induced pluripotent stem cell (hiPSC) transplantation is a versatile patient-specific regenerative approach for functional recovery after SCI. Injectable electroconductive hydrogel (ECH) can further enhance the cell transplantation efficacy through a minimally invasive manner as well as recapitulate the native bioelectrical microenvironment of neural tissue.
Netrin-1, an essential extracellular protein, has gained significant attention due to its pivotal role in guiding axon and cell migration during embryonic development. The fundamental significance of netrin-1 in developmental biology is reflected in its high conservation across different species as a part of the netrin family. The bifunctional nature of netrin-1 demonstrates its functional versatility, as it can function as either a repellent or an attractant according to the context and the expressed receptors on the target cells including the deleted in colorectal cancer (DCC), the uncoordinated-5 (UNC5), DSCAM, Neogenin-1, Adenosine A2b and Draxin receptors.
Department of Integrated Traditional Chinese and Western Medicine, Xiangya Hospital, Central South University, Jiangxi Hospital, National Reginal Center for Neurological Disease, Honggutan District, No.266 Fenghe North Avenue, Nanchang, 330038, Jiangxi, China.
Acute injury and secondary injury caused by traumatic brain injury (TBI) seriously threaten the health of patients. The purpose of this study was to investigate the role of β-Asarone in TBI-induced neuroinflammation and injury. In this work, the effects of β-Asarone on nerve injury and neuronal apoptosis were investigated in mice with TBI by controlled cortical impingement.
