Insights into the Role of Neuroinflammation in the Pathogenesis of Multiple Sclerosis

Abstract

Multiple sclerosis (MS) is a devastating disease, and with the increasing number of cases each year, it is becoming a significant socioeconomic burden for the affected people and the entire community. The aetiology of MS is largely unknown, but genetic susceptibility, exposure to infections and/or environmental toxicants are recognised as risk factors. MS is characterised by the appearance of lesions/plaques in the central nervous system, caused by destruction of the myelin sheet by auto-reactive T cells. Symptoms range from mild impairment of daily motor functions to severe sensory and cognitive disabilities necessitating mobility assistance, medical and support from caregivers. Due to the progressive nature of the disease, MS is gaining more attention and research to better understand its multifaceted pathogenesis. In the present review, we focus on some of the latest research related to the neuroinflammatory component of the disease, since it appears to play a critical role in MS pathogenesis. The goal is to shed more light on this specific domain of MS, in an attempt to assist in the identification of novel treatment trajectories and management plans.

The GPR17 Receptor—A Promising Goal for Therapy and a Potential Marker of the Neurodegenerative Process in Multiple Sclerosis

“…The pathogenesis of MS is characterized by a cascade of pathobiological events ranging from focal macrophage, leukocyte infiltration, and microglia activation, as well as the antigen-dependent activation of B lymphocytes and antibody-generation by plasma cells, to demyelination and chronic axonal degeneration [18,19]. The most likely immunological mechanisms involved in the pathogenesis of MS include molecular mimicry and the bystander activation effect [20]. Molecular mimicry is a phenomenon that involves the activation of B and T cells in response to actions directed against their own antigens by pathogen-like products that are similar in sequence and structure.…”

Role of the End-Point Mediators of Sympathoadrenal and Sympathoneural Stress Axes in the Pathogenesis of Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis

“…Multiple sclerosis (MS) is one of the most common neurological disorders and cause of disability of young adults (1)(2)(3). Patogenetically, MS is the prototype of the autoimmune inflammatory diseases of the central nervous system (CNS), and is characterized by breakdown of the blood-brain barrier (BBB), neuroinflammation, and axonal damage (4,5).…”

“…MS is multifactorial disease involving genetic traits and nongenetic triggers (1,2). Generally, physical and psychological stressors are important triggers of MS (10)(11)(12).…”

Daily Low Dose of Erythropoietin and Neuroinflammation

“…short mild form of it may be considered as rather repairing which contributes to the neurodevelopment, neuroprotection and neuroplasticity, yet its severe prolonged version may be debilitating to the patients. [5,6] This phenomenon, with its energy-consuming metabolic-demanding nature has been linked to the secondary pathological changes elicited in hypoglycemia [7] , the ischemic brain disorders [8,9] , intracerebral hemorrhage [10,11] , traumatic brain injury (TBI) [12,13] , Alzheimer's disease [14][15][16] , Parkinson's disease [17,18] and other neurodegenerative disorders such as amyotrophic lateral sclerosis (ALS) [19] , and multiple sclerosis (MS) [20,21] . It has recently been related to the neurobiological disorders like of epilepsy [22] , depression [23,24] , obsessivecompulsive disorder [25] and schizophrenia [26] .…”