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Fig. 1 | Multiple Sclerosis and Demyelinating Disorders

Fig. 1

From: The heritage of glatiramer acetate and its use in multiple sclerosis

Fig. 1

Immune-mediated pathological and modulatory pathways in multiple sclerosis (MS) and possible neuroprotective actions of glatiramer acetate (GA). GA has been shown to increase levels of neurotrophic factors (a), which are reduced in the serum and the cerebrospinal fluid of MS patients and whose actions include protection of neurons against pathological insults. By inducing specific populations of Th2 cells in the periphery, GA may promote neural growth and inhibit inflammatory demyelination resulting in loss of axons, neurons and oligodendrocytes (b). GA has also been shown to oppose glutamate excitotoxicity by restoring normal kinetic properties of glutamate-mediated synaptic transmission in the striatum (c). GA may produce this effect by blocking synaptic alterations due to TNF-alpha released by activated microglia (d). APC, antigen presenting cell; IFN, interferon; IL, interleukin; MMP, matrix metalloproteinase; TGF, transforming growth factor; Th, T helper; TNF, tumor necrosis factor; Treg, regulatory T cell (Modified with permission from [11])

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