A5090973235- Neuroinflammation and Neurodegeneration Mechanisms
- Neurogenesis and neuroplasticity mechanisms
- Cancer-related molecular mechanisms research
- interferon and immune responses
- Immune cells in cancer
- MicroRNA in disease regulation
- Nerve injury and regeneration
- Multiple Sclerosis Research Studies
- Signaling Pathways in Disease
- RNA regulation and disease
- Circular RNAs in diseases
- Telomeres, Telomerase, and Senescence
- Tissue Engineering and Regenerative Medicine
- PARP inhibition in cancer therapy
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Methane Hydrates and Related Phenomena
- Genomics and Phylogenetic Studies
- Microbial Community Ecology and Physiology
- Single-cell and spatial transcriptomics
- Extracellular vesicles in disease
- Immune Response and Inflammation
- Amyotrophic Lateral Sclerosis Research
- Systemic Lupus Erythematosus Research
- RNA Research and Splicing
- NF-κB Signaling Pathways
Montreal Neurological Institute and Hospital
2018-2025
McGill University
2018-2025
Lund University
2017-2024
University of Calgary
2022
Dysregulation of miRNAs has been observed in many neurodegenerative diseases, including multiple sclerosis. Morquette et al. show that overexpression miR-223-3p prevents accumulation axonal damage a rodent model sclerosis, part through regulation glutamate receptor signalling. Manipulation miRNA levels may have therapeutic potential.
Abstract Ependymal cells form a specialized brain–cerebrospinal fluid (CSF) interface and regulate local CSF microcirculation. It is becoming increasingly recognized that ependymal assume reactive state in response to aging disease, including conditions involving hypoxia, hydrocephalus, neurodegeneration, neuroinflammation. Yet what transcriptional signatures govern these states whether this reactivity shares any similarities with classical descriptions of glial (i.e., astrocytes) remain...
Highlights•RGCs demonstrate similar gene expression changes during EAE and aging•RGCs exhibit DNA damage, chromatin mark changes, nuclear lamina dystrophy in EAE•Patients with MS damage senescence-associated neurons•AAV2-OSK limits RGC death preserves visual acuity EAESummaryIn multiple sclerosis (MS), inflammation of the central nervous system results demyelination, neuroaxonal injury, cell death. However, molecular signals responsible for injury neurons are not fully characterized. Here,...
The role of senescence in disease contexts is complex, however there considerable evidence that depletion senescent cells improves outcomes a variety particularly related to aging, cognition, and neurodegeneration. Much research has shown previously inflammation can promote cellular senescence. Microglia are central nervous system innate immune cell undergo with aging during contribution microglia multiple sclerosis, an inflammatory neurodegenerative disease, not clear, but strongly...
Multiple sclerosis (MS) is an autoimmune, neurodegenerative disease but the molecular mechanisms underlying aspects of are poorly understood. microRNAs (miRNAs) powerful regulators gene expression that regulate numerous mRNAs simultaneously and can thus programs expression. Here, we describe miRNA in neurons captured from mice subjected to experimental autoimmune encephalomyelitis (EAE), a model central nervous system (CNS) inflammation. Lumbar motor retinal were laser EAE was assessed by...
In multiple sclerosis (MS), the invasion of central nervous system by peripheral immune cells is followed activation resident microglia and astrocytes. This cascade events results in demyelination, which triggers neuronal damage death. The molecular signals neurons responsible for this are not yet fully characterized. MS, retinal ganglion cell (RGCs) (CNS) undergo axonal injury phenomenon mirrored experimental autoimmune encephalomyelitis (EAE) mouse model MS. To understand landscape, we...
Abstract The role of senescence in disease contexts is complex, however there considerable evidence that depletion senescent cells improves outcomes a variety particularly related to aging, cognition, and neurodegeneration. Here, the effect bioinformatically-rationalized senolytic was tested experimental autoimmune encephalomyelitis (EAE) mouse model multiple sclerosis (MS). Single-cell analysis from brain tissue isolated mice subjected EAE identified microglia with strong signature...
Multiple sclerosis (MS) is an autoimmune and neurodegenerative disease driven by inflammation demyelination in the brain, spinal cord, optic nerve. Optic neuritis, characterized of nerve, a symptom many patients with MS. The nerve highway for visual information transmitted from retina to brain. It contains axons retinal ganglion cells (RGCs) that reside retina, myelin forming oligodendrocytes resident microglia astrocytes. Inflammation, demyelination, axonal degeneration are also present...
Abstract Multiple sclerosis (MS) is an autoimmune disease characterized by demyelination and neurodegeneration in the brain, spinal cord optic nerve. Neuronal degeneration death underlie progressive forms of MS cognitive dysfunction. damage triggered numerous harmful factors brain that engage diverse signalling cascades neurons thus therapeutic approaches to protect will need focus on agents can target broad biological processes. To spectrum signaling events mediate we have focused...
Microbially mediated processes in a given habitat tend to be catalyzed by abundant populations that are ecologically adapted exploit specific environmental characteristics. Typically, metabolic activities of rare limited but may stimulated response acute stressors. Community responses sudden changes temperature and pressure can include suppression activation different populations, these dynamics remain poorly understood. The permanently cold ocean floor hosts countless low-abundance microbes...
Abstract Multiple sclerosis (MS) is an immune-mediated disease characterized by chronic inflammation and damage to the central nervous system, substantial characterization of molecular signatures glial immune cells in has been conducted. However, comparatively less well signature pathologically inflamed neurons. Here, we accessed multi-omic high-throughput transcriptomic epigenomic data investigate neurons from progressive MS patients mice subjected experimental autoimmune encephalomyelitis...
Neuroinflammation can positively influence axon regeneration following injury in the central nervous system (CNS). Inflammation promotes release of neurotrophic molecules and stimulates intrinsic pro-regenerative molecular machinery neurons, but detailed mechanisms driving this effect are not fully understood. We evaluated how microRNAs regulated retinal neurons response to intraocular inflammation identify their potential role regeneration. found that miR-383-5p is downregulated ganglion...
The protein Nogo-A has been widely studied for its role in inhibiting axonal regeneration following injury to the central nervous system, but mechanism by which membrane-bound is presented intercellularly not fully understood. New research suggests that a highly inhibitory fragment of generated amyloid precursor protease BACE1 and on membranes exosomes spinal cord injury. This finding represents new mode through may exert effects system.