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Inflammation induced neurological handicap processes in multiple sclerosis: new insights from preclinical studies
Klaus G Petry1, Bruno Brochet, Vincent Dousset
1EA2966 Neurobiology of Myelin Pathologies/BP78, University of Bordeaux, 146 Rue Léo-Saignat, 33076 Bordeaux, France. klaus.petry@inserm.fr
Abstract:
Multiple sclerosis (MS) is described as originating from incompletely explained neuroinflammatory processes, dysfunction of neuronal repair mechanisms and chronicity of inflammation events. Blood-borne immune cell infiltration and microglia activation are causing both neuronal destruction and myelin loss, which are responsible for progressive motor deficiencies, organic and cognitive dysfunctions. MRI as a non-invasive imaging method offers various ways to visualise de- and remyelination, neuronal loss, leukocyte infiltration, blood-brain barrier modification and new sensors are emerging to detect inflammatory lesions at an early stage. We describe studies performed on experimental autoimmune encephalomyelitis (EAE) animal models of MS that shed new light on mechanisms of functional impairments to understand the neurological handicap in MS. We focus on examples of neuroinflammation-mediated inhibition of CNS repair involving adult neurogenesis in the sub-ventricular zone and hippocampus and such experimentally observed inhibitions could reflect deficient plasticity and activation of compensatory mechanisms in MS. In parallel with cognitive decline, organic deficits such as bladder dysfunction are described in most of MS patients. Neuropharmacological interventions, electrical stimulation of nerves, MRI and histopathology follow-up studies helped in understanding the operating events to remodel the neurological networks and to compensate the inflammatory lesions both in spinal cord and in cortical regions. At the molecular level, the local production of reactive products is a well-described phenomenon: oxidative species disturb cellular physiology and generate new molecular epitopes that could further promote immune reactions. The translational research from EAE animal models to MS patient cohorts helps in understanding the mechanisms of the neurological handicap and in development of new therapeutic concepts in MS.
Insights
Multiple sclerosis (MS) involves neuroinflammation and impaired repair, leading to motor and cognitive deficits. Research in animal models aids understanding of these mechanisms and developing new therapies for MS patients.
Area of Science:
- Neuroimmunology
- Neurobiology
- Neuropharmacology
Background:
- Multiple sclerosis (MS) pathogenesis involves complex neuroinflammatory processes, immune cell infiltration, and myelin loss, resulting in progressive neurological dysfunction.
- Dysfunctional neuronal repair mechanisms and chronic inflammation contribute to the debilitating effects of MS, including motor, cognitive, and organic deficits.
- Oxidative stress and molecular epitope generation at the cellular level exacerbate immune responses in MS.
Purpose of the Study:
- To elucidate the mechanisms underlying functional impairments and neurological handicaps in MS.
- To investigate the role of neuroinflammation in inhibiting central nervous system (CNS) repair, including adult neurogenesis.
- To explore translational research bridging experimental autoimmune encephalomyelitis (EAE) animal models and MS patient cohorts for therapeutic development.
Main Methods:
- Utilizing experimental autoimmune encephalomyelitis (EAE) animal models to study MS mechanisms.
- Employing magnetic resonance imaging (MRI) for non-invasive visualization of demyelination, neuronal loss, and inflammation.
- Applying neuropharmacological interventions, nerve electrical stimulation, and histopathology for network remodeling and lesion compensation studies.
Main Results:
- EAE models provide insights into neuroinflammation-mediated inhibition of CNS repair, affecting neurogenesis and plasticity.
- MRI and other follow-up studies help understand neurological network remodeling and compensation of inflammatory lesions.
- Molecular analysis reveals oxidative species contributing to cellular dysfunction and immune promotion in MS.
Conclusions:
- Translational research from EAE models to MS patients is crucial for understanding neurological handicaps.
- Understanding neuroinflammatory and repair deficits is key to developing novel therapeutic strategies for MS.
- Integrated approaches including imaging, pharmacology, and molecular studies advance MS treatment concepts.
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