Patients with multiple sclerosis (MS) often suffer from cognitive
dysfunction; the underlying mechanisms have not been fully elucidated. Recent
studies suggest that MS leads to heightened synaptic transmission and plasticity
in different brain areas, and therefore may contribute to the observed behavioral
abnormalities. Recent findings demonstrate synaptic plasticity changes in MS,
including evidence from animal models of experimental autoimmune
encephalomyelitis and human MS patients.
Keywords: Experimental autoimmune encephalomyelitis, inflammation, multiple sclerosis, N-methyl-D-aspartic acid, synaptic
plasticity, trophic factor.
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