2018 Aug 8
Division of Neurology, Department of Internal Medicine, University of South Carolina School of Medicine, Greeville
Can Aspirin Minimize Stroke Risk and New Lesion Formation in Multiple Sclerosis?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6092498/
Abstract
Even with increasing data implicating the venous side of the vascular tree of the brain in MS, no diagnostic or treatment protocol has addressed the risk of acute stroke in MS and no systematic study has documented the incidence or prevalence of acute strokein MS patients. Approximately 795,000 strokes occur in the U.S. each year-every 40 s, someone has a stroke and every 4 min, a person dies from a stroke. However, no large, prospective, multi-center study has investigated acute stroke incidence in MS patients either in the U.S. or internationally, leaving a gap in our understanding of the association between stroke and MS. Additionally, data on acute stroke in MS as determined by age, gender or ethnicity are unknown. To compound this further, the diagnosis and definition of acute stroke in MS remains poorly understood. A survey of published literature shows a few anecdotal reports of acute stroke occurring among MS patients, but most studies do not address the fundamental association between acute stroke and MS. Symptoms of acute stroke and MS can overlap and the lack of clear clinical/radiological criteria that alert the patient or clinician to the development of acute stroke in an MS patient compound the dilemma, even leading to the administration of IV alteplase in cases that are later diagnosed as either MS or having an "MS flare." Clinical trials that use aspirin in multiple sclerosis are urgently needed.
Aspirin
Aspirin
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Re: Aspirin
Free full text at https://www.ncbi.nlm.nih.gov/pmc/articl ... -00613.pdfPetr75 wrote:2018 Aug 8
Division of Neurology, Department of Internal Medicine, University of South Carolina School of Medicine, Greeville
Can Aspirin Minimize Stroke Risk and New Lesion Formation in Multiple Sclerosis?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6092498/
Re: Aspirin
2019 May 28
Division of Research and Development, Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois
Mode of Action of Aspirin in Experimental Autoimmune Encephalomyelitis
https://www.ncbi.nlm.nih.gov/pubmed/31140860
Abstract
Multiple sclerosis (MS) is a chronic and debilitating autoimmune disorder of the central nervous system in which the autoimmune T cells destroy myelin, thus causing lesion, damage, and neuronal dysfunction. Experimental autoimmune encephalomyelitis (EAE) is an animal model of MS that is particularly useful for testing new therapeutic approaches against MS. Aspirin (acetyl salicylic acid) is one of the oldest and widely used medicines in the world, and recently it has been shown that low-dose aspirin is capable of suppressing the disease process of EAE in mice. One of the root causes of this autoimmune disease process is the decrease and/or suppression of Foxp3-expressing anti-autoimmune regulatory T cells (Tregs) and associated increase in autoimmune T-helper 1 (Th1) and Th17 cells. Aspirin upregulates Tregs and decreases Th1 and Th17 responses. Accordingly, the suppression of Tregs abrogates the protective effect of aspirin on EAE, indicating that aspirin protects EAE via Tregs. While there are several mechanisms for the maintenance of Tregs under immune insults, aspirin increases the level of interleukin-11 (IL-11), an immunomodulatory cytokine, and IL-11 alone is sufficient to protect Tregs. Being a multifunctional molecule, aspirin stimulates the activation of cAMP-response element-binding (CREB) to promote the recruitment of CREB to the IL-11 gene promoter and stimulate the transcription of IL-11 in splenocytes. Therefore, it appears that low-dose aspirin protects EAE via CREB-mediated stimulation of IL-11-Treg pathway and that aspirin may have therapeutic importance in MS.
Division of Research and Development, Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois
Mode of Action of Aspirin in Experimental Autoimmune Encephalomyelitis
https://www.ncbi.nlm.nih.gov/pubmed/31140860
Abstract
Multiple sclerosis (MS) is a chronic and debilitating autoimmune disorder of the central nervous system in which the autoimmune T cells destroy myelin, thus causing lesion, damage, and neuronal dysfunction. Experimental autoimmune encephalomyelitis (EAE) is an animal model of MS that is particularly useful for testing new therapeutic approaches against MS. Aspirin (acetyl salicylic acid) is one of the oldest and widely used medicines in the world, and recently it has been shown that low-dose aspirin is capable of suppressing the disease process of EAE in mice. One of the root causes of this autoimmune disease process is the decrease and/or suppression of Foxp3-expressing anti-autoimmune regulatory T cells (Tregs) and associated increase in autoimmune T-helper 1 (Th1) and Th17 cells. Aspirin upregulates Tregs and decreases Th1 and Th17 responses. Accordingly, the suppression of Tregs abrogates the protective effect of aspirin on EAE, indicating that aspirin protects EAE via Tregs. While there are several mechanisms for the maintenance of Tregs under immune insults, aspirin increases the level of interleukin-11 (IL-11), an immunomodulatory cytokine, and IL-11 alone is sufficient to protect Tregs. Being a multifunctional molecule, aspirin stimulates the activation of cAMP-response element-binding (CREB) to promote the recruitment of CREB to the IL-11 gene promoter and stimulate the transcription of IL-11 in splenocytes. Therefore, it appears that low-dose aspirin protects EAE via CREB-mediated stimulation of IL-11-Treg pathway and that aspirin may have therapeutic importance in MS.
https://www.eboro.cz