A5066031802- Neuroinflammation and Neurodegeneration Mechanisms
- Neurogenesis and neuroplasticity mechanisms
- Multiple Sclerosis Research Studies
- Barrier Structure and Function Studies
- Inflammasome and immune disorders
- Extracellular vesicles in disease
- Inflammation biomarkers and pathways
- Galectins and Cancer Biology
- Neurological Disease Mechanisms and Treatments
- Autoimmune and Inflammatory Disorders Research
- Enzyme Catalysis and Immobilization
- Biomarkers in Disease Mechanisms
- Epigenetics and DNA Methylation
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- RNA modifications and cancer
- Various Chemistry Research Topics
- Signaling Pathways in Disease
- Ferroptosis and cancer prognosis
- Caveolin-1 and cellular processes
- Wound Healing and Treatments
- Genomics, phytochemicals, and oxidative stress
- Mesenchymal stem cell research
- Child Development and Digital Technology
- Nerve injury and regeneration
- Vector-borne infectious diseases
University of Calgary
2019-2024
Ontario Brain Institute
2021
Mount Royal University
2017
Abstract Remyelination following CNS demyelination restores rapid signal propagation and protects axons; however, its efficiency declines with increasing age. Both intrinsic changes in the oligodendrocyte progenitor cell population extrinsic factors lesion microenvironment of older subjects contribute to this decline. Microglia monocyte-derived macrophages are critical for successful remyelination, releasing growth clearing inhibitory myelin debris. Several studies have implicated delayed...
Remyelination failure in multiple sclerosis (MS) contributes to progression of disability. The deficient repair results from neuroinflammation and deposition inhibitors including chondroitin sulfate proteoglycans (CSPGs). Which CSPG member is repair-inhibitory or alters local inflammation exacerbate injury unknown. Here, we correlate high versican-V1 expression MS lesions with premyelinating oligodendrocytes, highlight its selective upregulation amongst members experimental autoimmune...
Aging is a significant risk factor associated with the progression of CNS neurodegenerative diseases including multiple sclerosis (MS). Microglia, resident macrophages parenchyma, are major population immune cells that accumulate in MS lesions. While they normally regulate tissue homeostasis and facilitate clearance neurotoxic molecules oxidized phosphatidylcholines (OxPCs), their transcriptome neuroprotective functions reprogrammed by aging. Thus, determining factors instigate aging...
Background Inflammation-exacerbated secondary brain injury and limited tissue regeneration are barriers to favourable prognosis after intracerebral haemorrhage (ICH). As a regulator of inflammation lipid metabolism, Liver X receptor (LXR) has the potential alter microglia/macrophage (M/M) phenotype, assist repair by promoting cholesterol efflux recycling from phagocytes. To support clinical translation, benefits enhanced LXR signalling examined in experimental ICH. Methods...
Multiple sclerosis (MS) is a neurodegenerative condition of the central nervous system (CNS). It associated with blood-brain barrier (BBB) breakdown and intravasation leukocytes, particularly monocyte-derived macrophages, into CNS. Pericytes are mural cells that encased within basement membrane vasculature, they contribute functionally to neurovascular unit. These play an important role in maintaining BBB integrity CNS homeostasis. However, critical pericytes mediating inflammation MS or its...
Impairment of oligodendrocytes and myelin contributes to neurological disorders including multiple sclerosis (MS), stroke Alzheimer's disease. Regeneration (remyelination) decreases the vulnerability demyelinated axons, but this repair process commonly fails with disease progression. A contributor inefficient remyelination is altered extracellular matrix (ECM) in lesions that remains be better defined. We have identified fibulin-2 (FBLN2) as a highly upregulated ECM component MS stroke,...
The pathophysiology of multiple sclerosis (MS) is contributed by B lymphocytes, macrophages, and microglia. Bruton tyrosine kinase (BTK) an intracellular enzyme within these cells that modulates their inflammatory properties. Thus, central nervous system-penetrant inhibitors BTK may counter immune dysregulation, this aspiration highlighted 11 phase 3 clinical trials in MS to inhibit enzyme. Despite the keen interest, spatial temporal elevation lesions its models not well characterized. We...
Abstract Oxidative stress promotes tissue injury in the central nervous system neurological disorders such as multiple sclerosis (MS). To protect against this, antioxidant enzymes including superoxide dismutase-1 (SOD1), heme oxygenase-1 (HO-1), peroxiredoxin-5 (PRDX5) and glutathione peroxidase-4 (GPX4) may be upregulated. However, whether enzyme elevation mouse models of neurodegeneration corresponds to their expression human diseases MS requires investigation. Here, we analyzed compared...
Neuroinflammation and neurodegeneration are key processes that mediate the development progression of neurological diseases. However, mechanisms modulating these in different diseases remain incompletely understood. Advances single cell based multi-omic analyses have helped to identify distinct molecular signatures such as Lgals3 is associated with neuroinflammation central nervous system (CNS). encodes galectin-3 (Gal3), a β-galactoside glycan binding glycoprotein frequently upregulated by...
Abstract Exercise affords broad benefits for people with multiple sclerosis (PwMS) including less fatigue, depression, and improved cognition. In animal models of (MS), exercise has been shown to improve remyelination, decrease blood–brain barrier permeability reduce leukocyte infiltration. Despite these many PwMS refrain from engaging in physical activity. This participation may be overcome by uncovering describing the mechanisms which promotes beneficial changes central nervous system...
Oxidized phosphatidylcholine (OxPC) found in multiple sclerosis brain lesions mediates neurodegeneration. Microglia are prominent responders to the OxPC insult, and thus, studying their protective or noxious functions is important help halt Here, we present protocols including cell isolation culture, animal surgeries, as well tissue processing study microglia response OxPC-mediated neurodegeneration vitro vivo. For complete details on use execution of this protocol, please refer Dong et al. (2021).
Tissue damage elicits a wound healing response of inflammation and remodeling aimed at restoring homeostasis. Dysregulation leads to accumulation effector cells extracellular matrix (ECM) components, collectively termed fibrosis, which impairs organ functions. Fibrosis the central nervous system, neurofibrosis, is major contributor lack neural regeneration it involves fibroblasts, microglia/macrophages astrocytes, their deposited ECM. Neurofibrosis occurs commonly across neurological...
<title>Abstract</title> Oxidized phosphatidylcholines (OxPC) are neurotoxic byproducts of oxidative stress elevated in the central nervous system (CNS) during progressive multiple sclerosis (P-MS). How OxPC contribute to pathophysiology P-MS is unclear. Here, we report that deposition CNS mice induces a chronic compartmentalized lesion with pathological features similar active lesions found P-MS. Using this new model, while microglia protected from neurodegeneration, they were also replaced...
Impairment of oligodendrocytes and myelin contributes to neurological disorders including multiple sclerosis (MS), stroke Alzheimer's disease1-4. Regeneration (remyelination) decreases the vulnerability demyelinated axons1,5,6 but this repair process commonly fails with disease progression7-9. A contributor inefficient remyelination is altered extracellular matrix (ECM) in lesions10-12 that remains be better defined. We have identified fibulin-2 (FBLN2) as a highly upregulated ECM component...