A5005586034- Neurogenesis and neuroplasticity mechanisms
- Spinal Cord Injury Research
- Nerve injury and regeneration
- Neuroinflammation and Neurodegeneration Mechanisms
- Spinal Dysraphism and Malformations
- Multiple Sclerosis Research Studies
- RNA regulation and disease
- Peripheral Neuropathies and Disorders
- RNA Research and Splicing
- Diet and metabolism studies
- Mesenchymal stem cell research
- Hereditary Neurological Disorders
- Inflammatory Myopathies and Dermatomyositis
- Neurological diseases and metabolism
- Adipose Tissue and Metabolism
- Glaucoma and retinal disorders
- Stress Responses and Cortisol
- Memory and Neural Mechanisms
- Neurogenetic and Muscular Disorders Research
- Nerve Injury and Rehabilitation
- Electrolyte and hormonal disorders
- Single-cell and spatial transcriptomics
- Viral Infections and Immunology Research
- Phagocytosis and Immune Regulation
- Muscle and Compartmental Disorders
Oregon Health & Science University
2018-2025
Center for Neurosciences
2019-2025
International Collaboration On Repair Discoveries
2008-2024
University of British Columbia
2008-2024
Institute of Zoology
2014-2017
Johns Hopkins Medicine
1989
Johns Hopkins University
1987-1989
Johns Hopkins Hospital
1987
Although colchicine has been used for centuries, its neuromuscular toxicity in humans is largely unrecognized. In this report we describe a characteristic syndrome of myopathy and neuropathy present 12 new cases the condition. Colchicine may occur patients with gout who take customary doses drug but have elevated plasma levels because altered renal function. It usually presents proximal weakness always elevation serum creatine kinase; both features remit within three to four weeks after...
Spontaneous remyelination occurs after spinal cord injury (SCI), but the extent of myelin repair and identity cells responsible remain incompletely understood contentious. We assessed cellular origin new by fate mapping platelet-derived growth factor receptor α (PDGFRα), Olig2+, P0+ following contusion SCI in mice. Oligodendrocyte precursor (OPCs; PDGFRα+) produced oligodendrocytes for <i>de novo</i> ensheathment ∼30% myelinated axons at epicenter 3 months SCI, demonstrating that these...
Remyelination occurs after spinal cord injury (SCI) but its functional relevance is unclear. We assessed the necessity of myelin regulatory factor (Myrf) in remyelination contusive SCI by deleting gene from platelet-derived growth receptor alpha positive (PDGFRα-positive) oligodendrocyte progenitor cells (OPCs) mice prior to SCI. While OPC proliferation and density are not altered Myrf inducible knockout SCI, accumulation new oligodendrocytes largely prevented. This greatly inhibits...
While neurodegeneration underlies the pathological basis for permanent disability in multiple sclerosis (MS), predictive biomarkers progression are lacking. Using an animal model of chronic MS, we find that synaptic injury precedes neuronal loss and identify thinning inner plexiform layer (IPL) as early feature inflammatory demyelination—prior to symptom onset. As domains anatomically segregated retina can be monitored longitudinally, hypothesize IPL could represent a biomarker MS....
Chronic demyelination and oligodendrocyte loss deprive neurons of crucial support. It is the degeneration their connections that drives progressive disability in demyelinating disease. However, whether chronic triggers neurodegeneration how it may do so remain unclear. We characterize two genetic mouse models inducible demyelination, one distinguished by effective remyelination other failure demyelination. While both lines feature axonal damage, mice with blocked have elevated neuronal...
Given the rising availability and use of genetically modified animals in basic science research, it has become increasingly important to develop clinically relevant models for spinal cord injury (SCI) mice. We developed a graded forceps crush model SCI mice that uses three different with spacers 0.25, 0.4, 0.55 mm, produce severe, moderate, mild injuries, respectively. Briefly, each mouse was subjected laminectomy T5-T7, 15-second using one those forceps, behavioral assessments, post-mortem...
In diseases such as multiple sclerosis, inflammation can injure the myelin sheath that surrounds axons, a process known demyelination. The spontaneous regeneration of myelin, called remyelination, is associated with restoration function and prevention axonal degeneration. Boosting remyelination therapeutic intervention promising new approach currently being tested in several clinical trials. endogenous regulation highly dependent on immune response. this review, we highlight cell biology its...
Cell transplantation for spinal cord injury (SCI) has largely been studied in sub-acute settings within 1–2 weeks of injury. In contrast, here we transplanted skin-derived precursors differentiated into Schwann cells (SKP-SCs) the contused rat 8 post-injury (wpi). Twenty-one later (29 wpi), SKP-SCs were found to have survived transplantation, integrated with host tissue, and mitigated formation a dense glial scar. Furthermore, filled much lesion sites greatly enhanced presence endogenous...
Abstract Neuroaxonal injury is a major driver of irreversible disability in demyelinating conditions. Accurate assessment the association between demyelination and axonal pathology critical for evaluating developing effective therapeutic approaches. Measuring neurofilament light chain (NfL) blood could putatively allow longitudinal monitoring neuroaxonal at “single protein resolution” with high pathological specificity. Here, we demonstrate robust tissue NfL-based severity inflammatory...
Abstract Spinal cord injury (SCI) results in substantial oligodendrocyte death and subsequent demyelination leading to white‐matter defects. Cell replacement strategies promote remyelination are under intense investigation; however, the optimal cell for transplantation remains be determined. We previously isolated a platelet‐derived growth factor (PDGF)‐responsive neural precursor (PRP) from ventral forebrain of fetal mice that primarily generates oligodendrocytes, but also astrocytes...
Although upper extremity functional recovery is a high priority for spinal cord injured patients with cervical injuries, few injury models have been developed in mice sustained deficits forelimb motor function. Here, we characterize dorsolateral funiculus (DLF) crush model mice, which ablates the rubrospinal tract (RST) unilaterally and thus allows correlation of to axonal regeneration assessment molecular targets. We conducted unilateral DLF injuries at levels C4 C6 assessed battery tests:...
Abstract Colchicine may produce a neuromuscular disorder even when given in customary doses. We report the electrodiagnostic features eight pathologically proven cases of colchicine‐induced myoneuropathy. Myopathic motor unit potentials and early recruitment were found proximal limb truncal muscles, frequently with fibrillations, positive sharp waves, or complex repetitive discharges. These electromyographic findings correlated course weakness, which rapidly resolved within weeks drug...
Because of the complex, multifaceted nature spinal cord injury (SCI), it is widely believed that a combination approaches will be superior to individual treatments. Therefore, we employed rat model cervical SCI evaluate four noninvasive treatments individually have been reported effective for acute during clinically relevant therapeutic time windows. These included ghrelin, ibuprofen, C16, and ketogenic diet (KD). were selected not only because their previously efficacy in models but also...
Chronic demyelination and oligodendrocyte loss deprive neurons of crucial support. It is the degeneration their connections that drives progressive disability in demyelinating disease. However, whether chronic triggers neurodegeneration how it may do so remain unclear. We characterize two genetic mouse models inducible demyelination, one distinguished by effective remyelination other failure demyelination. While both lines feature axonal damage, mice with blocked have elevated neuronal...
To determine whether standalone oligodendrocyte and myelin damage do not only increase neuronal vulnerability but are sufficient to cause neuroaxonal injury.
Abstract The development of therapeutic strategies to reduce impairments following spinal cord injury (SCI) motivates an active area research, because there are no effective therapies. One strategy is address injury‐induced demyelination spared axons by promoting endogenous or exogenous remyelination. However, previously, we showed that new myelin was not necessary regain hindlimb stepping moderate thoracic contusion in 3‐month‐old mice. present analysis investigated two potential mechanisms...
Spinal cord injury (SCI) in the mammalian CNS results formation of a glial scar around lesion site ([Fig. 1][1] A ). The limits axon regeneration but it also serves protective role by sequestering inflammatory cells to center, reducing tissue damage ([Herrmann et al.,
To analyze retinal signs of synaptic injury in an animal model inflammatory demyelination and neurodegeneration, i.e., EAE; to evaluate quantified assessment a layer with major component for predicting relentlessly progressive disability MS; use proteome-wide analysis deeply characterized MS population explore the possibility developing serum-based biomarker that can quantify global injury.