scholarly journals Metformin attenuated the autoimmune disease of the central nervous system in animal models of multiple sclerosis

2009 ◽  
Vol 183 (5) ◽  
pp. 3551.1-3551 ◽  
Author(s):  
N. Nath ◽  
M. Khan ◽  
M. K. Paintlia ◽  
M. N. Hoda ◽  
S. Giri
2009 ◽  
Vol 182 (12) ◽  
pp. 8005-8014 ◽  
Author(s):  
Narender Nath ◽  
Musfiquidin Khan ◽  
Manjeet K. Paintlia ◽  
Md Nasrul Hoda ◽  
Shailendra Giri

1999 ◽  
Vol 6 (3) ◽  
pp. 149-166 ◽  
Author(s):  
Paul Conlon ◽  
Jorge R. Oksenberg ◽  
Jingwu Zhang ◽  
Lawrence Steinman

Author(s):  
Amirhossein Azari Jafari ◽  
Seyyedmohammadsadeq Mirmoeeni

Multiple sclerosis (MS) is a chronic autoimmune disease affecting the central nervous system (CNS), caused by genetic and environmental factors. It is characterized by intermittent and recurrent episodes of inflammation that result in the demyelination and subsequent damage of the underlying axons present in the brain, optic nerve and spinal cord [1][2][3].


2016 ◽  
Vol 2 ◽  
pp. 205521731664998
Author(s):  
Kira Groen ◽  
Vicki E Maltby ◽  
Katherine A Sanders ◽  
Rodney J Scott ◽  
Lotti Tajouri ◽  
...  

Multiple sclerosis (MS) is an autoimmune disease characterised by lymphocytic infiltration of the central nervous system and subsequent destruction of myelin and axons. On the background of a genetic predisposition to autoimmunity, environmental triggers are assumed to initiate the disease. The majority of MS research has focused on the pathological involvement of lymphocytes and other immune cells, yet a paucity of attention has been given to erythrocytes, which may play an important role in MS pathology. The following review briefly summarises how erythrocytes may contribute to MS pathology through impaired antioxidant capacity and altered haemorheological features. The effect of disease-modifying therapies on erythrocytes is also reviewed. It may be important to further investigate erythrocytes in MS, as this could broaden the understanding of the pathological mechanisms of the disease, as well as potentially lead to the discovery of novel and innovative targets for future therapies.


2021 ◽  
Vol 23 (2) ◽  
pp. 165-169
Author(s):  
Viktoriia R. Cheredanova ◽  
◽  
Ivan A. Chabin ◽  
Raisa Ts. Bembeeva ◽  
◽  
...  

Multiple sclerosis (MS) is an autoimmune disease that affects the central nervous system and is a major cause of disability in able-bodied young people. Recently, the question of the effect of vitamin D on the risk of occurrence and clinical course of MS has been widely discussed. The review presents pathogenesis of this disease and estimated mechanisms of the effect of cholecalciferol on it, current data on the effect of vitamin D levels on the risk of MS, the course and outcome of this disease.


2019 ◽  
Vol 217 (1) ◽  
Author(s):  
Catriona A. Wagner ◽  
Pamela J. Roqué ◽  
Joan M. Goverman

Multiple sclerosis (MS) is an inflammatory, demyelinating disease of the central nervous system that is believed to have an autoimmune etiology. As MS is the most common nontraumatic disease that causes disability in young adults, extensive research has been devoted to identifying therapeutic targets. In this review, we discuss the current understanding derived from studies of patients with MS and animal models of how specific cytokines produced by autoreactive CD4 T cells contribute to the pathogenesis of MS. Defining the roles of these cytokines will lead to a better understanding of the potential of cytokine-based therapies for patients with MS.


2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Bharath Wootla ◽  
Makoto Eriguchi ◽  
Moses Rodriguez

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS) with varied clinical presentations and heterogeneous histopathological features. The underlying immunological abnormalities in MS lead to various neurological and autoimmune manifestations. There is strong evidence that MS is, at least in part, an immune-mediated disease. There is less evidence that MS is a classical autoimmune disease, even though many authors state this in the description of the disease. We show the evidence that both supports and refutes the autoimmune hypothesis. In addition, we present an alternate hypothesis based on virus infection to explain the pathogenesis of MS.


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